Structured Review

LC Laboratories doxorubicin
Ginger-derived nanovectors (GDNVs) can be used as a drug carrier and load therapeutic <t>agent-doxorubicin</t> (Dox) efficiency. ( a ) Loading efficiency of Dox in GDNVs was measured. 200 μg of Dox solution was added into the ginger lipid film (the lipid
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1) Product Images from "Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy"

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy

Journal: Molecular Therapy

doi: 10.1038/mt.2016.159

Ginger-derived nanovectors (GDNVs) can be used as a drug carrier and load therapeutic agent-doxorubicin (Dox) efficiency. ( a ) Loading efficiency of Dox in GDNVs was measured. 200 μg of Dox solution was added into the ginger lipid film (the lipid
Figure Legend Snippet: Ginger-derived nanovectors (GDNVs) can be used as a drug carrier and load therapeutic agent-doxorubicin (Dox) efficiency. ( a ) Loading efficiency of Dox in GDNVs was measured. 200 μg of Dox solution was added into the ginger lipid film (the lipid

Techniques Used: Derivative Assay

Evaluation the apoptosis in Colon-26 cells induced by free doxorubicin (Dox) and Dox-GDNVs using Annexin V-FITC/PI staining and ECIS technology. ( a ) Control group. ( b ) Free Dox group. ( c ) Dox-GDNVs group. Cells were treated with three different Dox concentrations
Figure Legend Snippet: Evaluation the apoptosis in Colon-26 cells induced by free doxorubicin (Dox) and Dox-GDNVs using Annexin V-FITC/PI staining and ECIS technology. ( a ) Control group. ( b ) Free Dox group. ( c ) Dox-GDNVs group. Cells were treated with three different Dox concentrations

Techniques Used: Staining, Electric Cell-substrate Impedance Sensing

2) Product Images from "Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling"

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-015-0466-4

Anoikis-resistant OS cells show resistance to standard OS chemotherapies. Dose-response curves for cells grown under AI or adherent conditions treated with doxorubicin (top panel) or cisplatin (bottom panel) in a set of serial dilutions for 72 hours. Cell viability was determined as a percentage of the untreated control (0 μM doxorubicin or cisplatin).
Figure Legend Snippet: Anoikis-resistant OS cells show resistance to standard OS chemotherapies. Dose-response curves for cells grown under AI or adherent conditions treated with doxorubicin (top panel) or cisplatin (bottom panel) in a set of serial dilutions for 72 hours. Cell viability was determined as a percentage of the untreated control (0 μM doxorubicin or cisplatin).

Techniques Used:

5-azaC treatment inhibits anchorage-independent OS cell growth while sensitizing to doxorubicin. A/B : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug and allowed to grow for 4 days. 5-azaC treatment decreased the cells ability to form spheres (A) and resulted in a significant decrease in cell viability (B) . C/D : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug. 24 hours later the cells were treated with one concentration from a serial dilution of doxorubicin, with cell viability being measured after an additional 72 hours. 5-azaC treatment resulted in a left-shift in the doxorubicin dose-response curve (C) and a significant decrease in the percent IC 50 relative to vehicle alone (D) . Asterisks indicate statistical significance (*p
Figure Legend Snippet: 5-azaC treatment inhibits anchorage-independent OS cell growth while sensitizing to doxorubicin. A/B : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug and allowed to grow for 4 days. 5-azaC treatment decreased the cells ability to form spheres (A) and resulted in a significant decrease in cell viability (B) . C/D : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug. 24 hours later the cells were treated with one concentration from a serial dilution of doxorubicin, with cell viability being measured after an additional 72 hours. 5-azaC treatment resulted in a left-shift in the doxorubicin dose-response curve (C) and a significant decrease in the percent IC 50 relative to vehicle alone (D) . Asterisks indicate statistical significance (*p

Techniques Used: Concentration Assay, Serial Dilution

3) Product Images from "Label-Free Recognition of Drug Resistance via Impedimetric Screening of Breast Cancer Cells"

Article Title: Label-Free Recognition of Drug Resistance via Impedimetric Screening of Breast Cancer Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0057423

Drug response of MCF-7 WT cells and MCF-7 DOX cells to 20 µM doxorubicin during 24 h at LF (10 kHz). Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h. The impedance drops sharply at LF for MCF-7 WT cells, indicating that 20 µM doxorubicin is strong enough to induce toxic effects, while cells in the absence of drug (control) were healthy and LF signal was relatively unchanged. On the other hand, MCF-7 DOX cells displayed increasing impedance compared to their control indicating resistance to this drug concentration and demonstrating the substantial differences in the drug response of MCF-7 WT cells and their drug resistant phenotypes.
Figure Legend Snippet: Drug response of MCF-7 WT cells and MCF-7 DOX cells to 20 µM doxorubicin during 24 h at LF (10 kHz). Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h. The impedance drops sharply at LF for MCF-7 WT cells, indicating that 20 µM doxorubicin is strong enough to induce toxic effects, while cells in the absence of drug (control) were healthy and LF signal was relatively unchanged. On the other hand, MCF-7 DOX cells displayed increasing impedance compared to their control indicating resistance to this drug concentration and demonstrating the substantial differences in the drug response of MCF-7 WT cells and their drug resistant phenotypes.

Techniques Used: Concentration Assay

Effect of stimulatory non-toxic drug concentrations on MCF-7 DOX. a) MCF-7 DOX exhibits a concentration-dependent increase in impedance magnitudes during drug treatment with nontoxic concentrations. The plot was fitted by nonlinear regression using exponential decay equation only for visual presentation. b) Impedance magnitudes vs. time plots of MCF-7 DOX cells when 20 µM doxorubicin was applied for 48 h and followed by medium washing for 24 h. This shows that the impedance increase is reversible when the drug is removed. c) Temporal evolution of |Z| when resistant cells were exposed to 5 µM doxorubicin for 24 h, followed by 20 µM drug concentration for 24 h, then medium washing as a last step for 1 h. This shows that the impedance increase can be sequentially added up; once the stress on cells is removed, the initial state of extracellular environment is reobtained. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.
Figure Legend Snippet: Effect of stimulatory non-toxic drug concentrations on MCF-7 DOX. a) MCF-7 DOX exhibits a concentration-dependent increase in impedance magnitudes during drug treatment with nontoxic concentrations. The plot was fitted by nonlinear regression using exponential decay equation only for visual presentation. b) Impedance magnitudes vs. time plots of MCF-7 DOX cells when 20 µM doxorubicin was applied for 48 h and followed by medium washing for 24 h. This shows that the impedance increase is reversible when the drug is removed. c) Temporal evolution of |Z| when resistant cells were exposed to 5 µM doxorubicin for 24 h, followed by 20 µM drug concentration for 24 h, then medium washing as a last step for 1 h. This shows that the impedance increase can be sequentially added up; once the stress on cells is removed, the initial state of extracellular environment is reobtained. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.

Techniques Used: Concentration Assay

Concentration-response curves are obtained by plotting |Z| at 2 MHz after exposing the cells to various concentrations of doxorubicin. The data was fitted to a sigmoid model. Based on the resulting fit, IC 50 values were obtained as 0.4 µM and 70 µM for MCF-7 WT and MCF-7 DOX respectively. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.
Figure Legend Snippet: Concentration-response curves are obtained by plotting |Z| at 2 MHz after exposing the cells to various concentrations of doxorubicin. The data was fitted to a sigmoid model. Based on the resulting fit, IC 50 values were obtained as 0.4 µM and 70 µM for MCF-7 WT and MCF-7 DOX respectively. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.

Techniques Used: Concentration Assay

Normalized |Z| vs. different concentrations of doxorubicin at LF (10 kHz) and HF (2 MHz) for a) MCF-7 WT: the LF and HF signals exhibit different profiles with respect to different drug concentrations. At low drug concentrations, the LF signal increased when HF signal was unaltered. At mild drug concentrations such as 0.2 µM doxorubicin, the LF signal decreased with no change in HF signal. At high drug concentrations such as 20 µM and 40 µM doxorubicin both LF and HF signal decreased sharply, showing similar kinetics. b) MCF-7 DOX: the LF signal increases at non-lethal drug concentrations when HF signal exhibited a slight increase. At high drug concentrations such as 40 µM and higher, the LF and HF signal displayed similar impedance profiles and dropped sharply. The plots were fitted by nonlinear regression based on the equation for bell-shaped concentration response only for visual presentation. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.
Figure Legend Snippet: Normalized |Z| vs. different concentrations of doxorubicin at LF (10 kHz) and HF (2 MHz) for a) MCF-7 WT: the LF and HF signals exhibit different profiles with respect to different drug concentrations. At low drug concentrations, the LF signal increased when HF signal was unaltered. At mild drug concentrations such as 0.2 µM doxorubicin, the LF signal decreased with no change in HF signal. At high drug concentrations such as 20 µM and 40 µM doxorubicin both LF and HF signal decreased sharply, showing similar kinetics. b) MCF-7 DOX: the LF signal increases at non-lethal drug concentrations when HF signal exhibited a slight increase. At high drug concentrations such as 40 µM and higher, the LF and HF signal displayed similar impedance profiles and dropped sharply. The plots were fitted by nonlinear regression based on the equation for bell-shaped concentration response only for visual presentation. Data points (mean ± SEM, n = 5) were normalized to the magnitude value at t = 0 h.

Techniques Used: Concentration Assay

4) Product Images from "Doxorubicin Blocks Cardiomyocyte Autophagic Flux by Inhibiting Lysosome Acidification"

Article Title: Doxorubicin Blocks Cardiomyocyte Autophagic Flux by Inhibiting Lysosome Acidification

Journal: Circulation

doi: 10.1161/CIRCULATIONAHA.115.017443

Doxorubicin impairs V-ATPase function in NRVM. ( A ) Lysosome re-acidification in live cardiomyocytes after NH 4 Cl-induced alkalinization. Dextran, Oregon Green 514 was used to monitor relative change of lysosomal pH. Representative recordings of the fluorescence ratio of different treatment groups are illustrated. ( B) Fluorescence ratios of different treatment groups were compared at different time points (t = 0 s, 1000 s, 2000 s) under basal conditions, during lysosomal alkanization, and during re-acidification. N = 22–25 cells in 5 independent experiments. Repeated measures ANOVA and subsequent Tukey post hoc tests were performed for statistical analysis. *, p
Figure Legend Snippet: Doxorubicin impairs V-ATPase function in NRVM. ( A ) Lysosome re-acidification in live cardiomyocytes after NH 4 Cl-induced alkalinization. Dextran, Oregon Green 514 was used to monitor relative change of lysosomal pH. Representative recordings of the fluorescence ratio of different treatment groups are illustrated. ( B) Fluorescence ratios of different treatment groups were compared at different time points (t = 0 s, 1000 s, 2000 s) under basal conditions, during lysosomal alkanization, and during re-acidification. N = 22–25 cells in 5 independent experiments. Repeated measures ANOVA and subsequent Tukey post hoc tests were performed for statistical analysis. *, p

Techniques Used: Fluorescence

Doxorubicin cardiotoxicity is exacerbated in αMHC-Beclin 1 transgenic mice. ( A ) Autophagic flux in WT and αMHC-Beclin 1 transgenic (Beclin 1 Tg) mouse hearts examined by immunoblotting LC3 and p62 24 hours after doxorubicin (5 mg/kg) injection, with or without Bafilomycin A1 treatment. N = 4 per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. *, p
Figure Legend Snippet: Doxorubicin cardiotoxicity is exacerbated in αMHC-Beclin 1 transgenic mice. ( A ) Autophagic flux in WT and αMHC-Beclin 1 transgenic (Beclin 1 Tg) mouse hearts examined by immunoblotting LC3 and p62 24 hours after doxorubicin (5 mg/kg) injection, with or without Bafilomycin A1 treatment. N = 4 per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. *, p

Techniques Used: Transgenic Assay, Mouse Assay, Injection

Doxorubicin induces autolysosome accumulation in mouse heart. ( A ) Representative fluorescence images of heart tissue sections from CAG-RFP-GFP-LC3 transgenic mice 24 hours after one-dose DOX injection. Bafilomycin A1 (1.5 mg/kg, BafA1) was injected intraperitoneally 2 hours before sacrifice. Autophagosome (yellow puncta) and autolysosome (red puncta) numbers in heart after DOX/NS treatment were calculated. N = 4–5 hearts per group with 6 microscopic fields (14,000 μm 2 ) per heart section analyzed. Scale bar, 20 μm. NS, normal saline. DOX, doxorubicin. HPF, high-power field. One-way ANOVA and subsequent Tukey tests were performed for analyzing autophagosome numbers and autolysosome numbers respectively, among different groups. *, p
Figure Legend Snippet: Doxorubicin induces autolysosome accumulation in mouse heart. ( A ) Representative fluorescence images of heart tissue sections from CAG-RFP-GFP-LC3 transgenic mice 24 hours after one-dose DOX injection. Bafilomycin A1 (1.5 mg/kg, BafA1) was injected intraperitoneally 2 hours before sacrifice. Autophagosome (yellow puncta) and autolysosome (red puncta) numbers in heart after DOX/NS treatment were calculated. N = 4–5 hearts per group with 6 microscopic fields (14,000 μm 2 ) per heart section analyzed. Scale bar, 20 μm. NS, normal saline. DOX, doxorubicin. HPF, high-power field. One-way ANOVA and subsequent Tukey tests were performed for analyzing autophagosome numbers and autolysosome numbers respectively, among different groups. *, p

Techniques Used: Fluorescence, Transgenic Assay, Mouse Assay, Injection

Doxorubicin inhibits autophagic flux in cultured neonatal rat ventricular myocytes (NRVM). ( A ) Time-dependent blockage of autophagic flux by doxorubicin. Quantification of LC3-II/GAPDH and p62/GAPDH were analyzed in 3 independent experiments. ( B ) Long-lived protein degradation assay revealed that doxorubicin decreased autophagic protein degradation in NRVM. N = 3 independent experiments in duplicates. ( C ) Representative fluorescence images of NRVM expressing RFP-GFP-LC3 and treated with DOX for 8 hours. Nuclei were stained with DAPI. Numbers of autophagosomes and autolysosomes in each cell were quantified. N = 40–50 cells per group. Scale bar, 10 μm. ( D ) Representative transmission electron microscopy images of cardiomyocytes treated overnight with doxorubicin. Arrows, lysosomes/autolysosomes containing electron-dense contents; Arrowhead, autophagosome. Scale bars, 1 μm in left- and 0.5 μm right-side images, respectively. Two-way ANOVA and subsequent Tukey tests were performed for statistical analysis. *, p
Figure Legend Snippet: Doxorubicin inhibits autophagic flux in cultured neonatal rat ventricular myocytes (NRVM). ( A ) Time-dependent blockage of autophagic flux by doxorubicin. Quantification of LC3-II/GAPDH and p62/GAPDH were analyzed in 3 independent experiments. ( B ) Long-lived protein degradation assay revealed that doxorubicin decreased autophagic protein degradation in NRVM. N = 3 independent experiments in duplicates. ( C ) Representative fluorescence images of NRVM expressing RFP-GFP-LC3 and treated with DOX for 8 hours. Nuclei were stained with DAPI. Numbers of autophagosomes and autolysosomes in each cell were quantified. N = 40–50 cells per group. Scale bar, 10 μm. ( D ) Representative transmission electron microscopy images of cardiomyocytes treated overnight with doxorubicin. Arrows, lysosomes/autolysosomes containing electron-dense contents; Arrowhead, autophagosome. Scale bars, 1 μm in left- and 0.5 μm right-side images, respectively. Two-way ANOVA and subsequent Tukey tests were performed for statistical analysis. *, p

Techniques Used: Cell Culture, Degradation Assay, Fluorescence, Expressing, Staining, Transmission Assay, Electron Microscopy

Doxorubicin inhibits lysosomal acidification in NRVM. ( A ) Doxorubicin inhibited activities of lysosomal enzymes cathepsin B and cathepsin L in live cardiomyocytes examined by FACS. Quantifications were based on 4 independent experiments. ( B ) Lysotracker Red (DND-99, 100nM for 30 minutes) positive puncta in cytosol was significantly reduced after 8-hour doxorubicin treatment (the nuclear fluorescence in doxorubicin-treated NRVM derives from doxorubicin). Bafilomycin A1 treatment (50 nM for 2 hours) served as a positive control. ( C ) Doxorubicin decreased Lysosensor DND-189 fluorescence, determined by FACS. Bafilomycin A1 (50 nM for 2 hours) and NH 4 Cl (10 mM for 0.5 hour) are positive controls. N = 3 independent experiments in duplicates. ( D ) Doxorubicin (overnight treatment) increased lysosomal pH. Lysosomal pH was examined using Dextran, Oregon Green 514. Bafilomycin A1 and NH 4 Cl are positive controls. Three independent experiments with a total of 100–120 cells were examined. CtsB, cathepsin B. CtsL, cathespsin L. Scale bar, 10 μm. T-test between NS group and other treatment groups was performed for statistical analysis. *, p
Figure Legend Snippet: Doxorubicin inhibits lysosomal acidification in NRVM. ( A ) Doxorubicin inhibited activities of lysosomal enzymes cathepsin B and cathepsin L in live cardiomyocytes examined by FACS. Quantifications were based on 4 independent experiments. ( B ) Lysotracker Red (DND-99, 100nM for 30 minutes) positive puncta in cytosol was significantly reduced after 8-hour doxorubicin treatment (the nuclear fluorescence in doxorubicin-treated NRVM derives from doxorubicin). Bafilomycin A1 treatment (50 nM for 2 hours) served as a positive control. ( C ) Doxorubicin decreased Lysosensor DND-189 fluorescence, determined by FACS. Bafilomycin A1 (50 nM for 2 hours) and NH 4 Cl (10 mM for 0.5 hour) are positive controls. N = 3 independent experiments in duplicates. ( D ) Doxorubicin (overnight treatment) increased lysosomal pH. Lysosomal pH was examined using Dextran, Oregon Green 514. Bafilomycin A1 and NH 4 Cl are positive controls. Three independent experiments with a total of 100–120 cells were examined. CtsB, cathepsin B. CtsL, cathespsin L. Scale bar, 10 μm. T-test between NS group and other treatment groups was performed for statistical analysis. *, p

Techniques Used: FACS, Fluorescence, Positive Control

Beclin 1 +/− mice are protected from doxorubicin cardiotoxicity. ( A ) Autophagic flux inhibition by doxorubicin was rescued in Beclin 1 +/− mouse hearts. LC3 and p62 levels were evaluated by Western blotting in hearts 24 hours after doxorubicin (5 mg/kg) injection, with or without BafA1 treatment. N = 4 per group. Two-way ANOVA and subsequent Tukey tests were performed for statistical analysis. *, p
Figure Legend Snippet: Beclin 1 +/− mice are protected from doxorubicin cardiotoxicity. ( A ) Autophagic flux inhibition by doxorubicin was rescued in Beclin 1 +/− mouse hearts. LC3 and p62 levels were evaluated by Western blotting in hearts 24 hours after doxorubicin (5 mg/kg) injection, with or without BafA1 treatment. N = 4 per group. Two-way ANOVA and subsequent Tukey tests were performed for statistical analysis. *, p

Techniques Used: Mouse Assay, Inhibition, Western Blot, Injection

Doxorubicin inhibits autophagic flux in mouse heart. ( A ) Temporal changes in LC3-II, p62 and Beclin 1 protein levels after one dose of doxorubicin. Hearts were harvested at different time points after IV injection of doxorubicin (5 mg/kg, DOX) or normal saline (NS). Immunoblotting of LC3, p62 and Beclin 1 in heart lysates and quantifications are shown. N = 3–5 mice per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare doxorubicin-treated animals with control animals. ( B ) Transcript abundance of multiple autophagy-related genes (including p62/Sqstm1 ) at different time points after doxorubicin treatment. N = 3–6 mice per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare doxorubicin-treated mice with control mice. ( C ) Doxorubicin inhibited cardiac autophagic flux. Bafilomycin A1 (1.5 mg/kg, BafA1) was administered 22 hours after one dose of doxorubicin (5 mg/kg) to assess acute autophagic changes, as well as 22 hours and 7 days after 4 serial doxorubicin injections to assess autophagic changes in a chronic doxorubicin model. Immunoblotting of LC3 is shown. N = 4–5 per group. Asterisks on the schematics point to time points of assessment of autophagic flux. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. ( D ) Autophagic flux was increased in mouse hearts 4 weeks after the fourth injection of DOX. N = 6 per group. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. *, p
Figure Legend Snippet: Doxorubicin inhibits autophagic flux in mouse heart. ( A ) Temporal changes in LC3-II, p62 and Beclin 1 protein levels after one dose of doxorubicin. Hearts were harvested at different time points after IV injection of doxorubicin (5 mg/kg, DOX) or normal saline (NS). Immunoblotting of LC3, p62 and Beclin 1 in heart lysates and quantifications are shown. N = 3–5 mice per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare doxorubicin-treated animals with control animals. ( B ) Transcript abundance of multiple autophagy-related genes (including p62/Sqstm1 ) at different time points after doxorubicin treatment. N = 3–6 mice per group. One-way ANOVA analysis followed by Tukey post hoc test was used to compare doxorubicin-treated mice with control mice. ( C ) Doxorubicin inhibited cardiac autophagic flux. Bafilomycin A1 (1.5 mg/kg, BafA1) was administered 22 hours after one dose of doxorubicin (5 mg/kg) to assess acute autophagic changes, as well as 22 hours and 7 days after 4 serial doxorubicin injections to assess autophagic changes in a chronic doxorubicin model. Immunoblotting of LC3 is shown. N = 4–5 per group. Asterisks on the schematics point to time points of assessment of autophagic flux. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. ( D ) Autophagic flux was increased in mouse hearts 4 weeks after the fourth injection of DOX. N = 6 per group. Two-way ANOVA analysis followed by Tukey post hoc test was used to compare multiple groups. *, p

Techniques Used: IV Injection, Mouse Assay, Injection

5) Product Images from "Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA"

Article Title: Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2017.5060

Dose effect of DXR on cytotoxicity in HeLa cells at 24 h after transfection with PLK1 or HSF1 siRNA. The cells were transfected with 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA for 24 h and then treated with various concentrations of DXR for an additional 6 h. The medium containing DXR was changed for fresh medium without DXR, and then incubated for another 18 h. The number of viable cells was determined using a Cell Counting kit-8 assay. Data are presented as the mean + standard deviation (n=4). DXR, doxorubicin; PLK1, polo-like kinase 1; HSF1, heat shock transcription factor 1; siRNA, small interfering RNA; Cont, control; conc, concentration.
Figure Legend Snippet: Dose effect of DXR on cytotoxicity in HeLa cells at 24 h after transfection with PLK1 or HSF1 siRNA. The cells were transfected with 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA for 24 h and then treated with various concentrations of DXR for an additional 6 h. The medium containing DXR was changed for fresh medium without DXR, and then incubated for another 18 h. The number of viable cells was determined using a Cell Counting kit-8 assay. Data are presented as the mean + standard deviation (n=4). DXR, doxorubicin; PLK1, polo-like kinase 1; HSF1, heat shock transcription factor 1; siRNA, small interfering RNA; Cont, control; conc, concentration.

Techniques Used: Transfection, Incubation, Cell Counting, Standard Deviation, Small Interfering RNA, Concentration Assay

6) Product Images from "Analysis of redox and apoptotic effects of anthracyclines to delineate a cardioprotective strategy"

Article Title: Analysis of redox and apoptotic effects of anthracyclines to delineate a cardioprotective strategy

Journal: Cancer chemotherapy and pharmacology

doi: 10.1007/s00280-015-2879-4

Anthracyclines induce cytotoxic changes in cardiac tissue and increase ROS levels in monocytes. Doxorubicin cumulative dose is correlated with ROS levels
Figure Legend Snippet: Anthracyclines induce cytotoxic changes in cardiac tissue and increase ROS levels in monocytes. Doxorubicin cumulative dose is correlated with ROS levels

Techniques Used:

7) Product Images from "ERBB2 Deficiency Alters an E2F-1-Dependent Adaptive Stress Response and Leads to Cardiac Dysfunction"

Article Title: ERBB2 Deficiency Alters an E2F-1-Dependent Adaptive Stress Response and Leads to Cardiac Dysfunction

Journal: Molecular and Cellular Biology

doi: 10.1128/MCB.00895-14

Effect of doxorubicin treatment on cardiac function of WT and ERBB2 hypomorphic mice. (A) Representative M-mode echocardiographic images from 2-month-old WT and ERBB2 KI mice treated with doxorubicin (10 mg/kg) or saline solution as control (vehicle).
Figure Legend Snippet: Effect of doxorubicin treatment on cardiac function of WT and ERBB2 hypomorphic mice. (A) Representative M-mode echocardiographic images from 2-month-old WT and ERBB2 KI mice treated with doxorubicin (10 mg/kg) or saline solution as control (vehicle).

Techniques Used: Mouse Assay

Effect of doxorubicin and 7.16.4 cotreatment on cardiac function in mice. (A) Representative M-mode echocardiographic images of 2-month-old WT-treated mice. (B) Percentages of left ventricular ejection fraction (LVEF) in 2-month-old treated WT animals.
Figure Legend Snippet: Effect of doxorubicin and 7.16.4 cotreatment on cardiac function in mice. (A) Representative M-mode echocardiographic images of 2-month-old WT-treated mice. (B) Percentages of left ventricular ejection fraction (LVEF) in 2-month-old treated WT animals.

Techniques Used: Mouse Assay

8) Product Images from "Chemotherapy induces adaptive drug resistance and metastatic potentials via phenotypic CXCR4-expressing cell state transition in ovarian cancer"

Article Title: Chemotherapy induces adaptive drug resistance and metastatic potentials via phenotypic CXCR4-expressing cell state transition in ovarian cancer

Journal: PLoS ONE

doi: 10.1371/journal.pone.0171044

Using a combination of doxorubicin and CXCR4-KLA could synergistically inhibit invasion, migration, and colonization of OVC. (A-C) Representative images showing the wound healing, migration, and colony formation assays on A2780/ADR, CXCR4 High , and CXCR4 Low . The cells were treated with vehicle alone, doxorubicin alone, CXCR4-KLA alone and a combination of the drug and peptide. (D-F) The results were also presented quantitatively to reflect the percentage and number of cells that invaded the wounds and migrated through the chambers, as well as the number of colonies formed. The results expressed on the graph represent the means ± SD of three independent experiments (t-test, * p
Figure Legend Snippet: Using a combination of doxorubicin and CXCR4-KLA could synergistically inhibit invasion, migration, and colonization of OVC. (A-C) Representative images showing the wound healing, migration, and colony formation assays on A2780/ADR, CXCR4 High , and CXCR4 Low . The cells were treated with vehicle alone, doxorubicin alone, CXCR4-KLA alone and a combination of the drug and peptide. (D-F) The results were also presented quantitatively to reflect the percentage and number of cells that invaded the wounds and migrated through the chambers, as well as the number of colonies formed. The results expressed on the graph represent the means ± SD of three independent experiments (t-test, * p

Techniques Used: Migration, T-Test

Chemotherapy transiently induced the CXCR4 High cell state transition in human OVC. (A) Representative FACS analysis showed that A2780/ADR displays a higher percentage of CXCR4 High than A2780. Cells were stained with fluorescently labeled anti-CD44, anti-CD133, or anti-CXCR4, and also with anti-CD24. The numbers in the quadrants indicate the average percentage of CXCR4 High . (B) Chemotherapy reversibly induced CXCR4 High in A2780 and SKOV-3. A comparison of the changes in the cell population 72 h after treatment with suboptimal concentrations of cisplatin (1 μM), doxorubicin (10 nM), and paclitaxel (100 pM). At 72 h after withdrawing the drugs, the percentage of CXCR4 High returned to the basal level. (C and D) The drug-induced CXCR4 High was confirmed using western blot and real-time PCR analysis of the CXCR4 expression in the cell lysates. All the results represent means ± SD of three independent experiments (t-test, * p
Figure Legend Snippet: Chemotherapy transiently induced the CXCR4 High cell state transition in human OVC. (A) Representative FACS analysis showed that A2780/ADR displays a higher percentage of CXCR4 High than A2780. Cells were stained with fluorescently labeled anti-CD44, anti-CD133, or anti-CXCR4, and also with anti-CD24. The numbers in the quadrants indicate the average percentage of CXCR4 High . (B) Chemotherapy reversibly induced CXCR4 High in A2780 and SKOV-3. A comparison of the changes in the cell population 72 h after treatment with suboptimal concentrations of cisplatin (1 μM), doxorubicin (10 nM), and paclitaxel (100 pM). At 72 h after withdrawing the drugs, the percentage of CXCR4 High returned to the basal level. (C and D) The drug-induced CXCR4 High was confirmed using western blot and real-time PCR analysis of the CXCR4 expression in the cell lysates. All the results represent means ± SD of three independent experiments (t-test, * p

Techniques Used: FACS, Staining, Labeling, Western Blot, Real-time Polymerase Chain Reaction, Expressing, T-Test

CXCR4 High can be a useful target for OVC treatment. (A) CXCR4-KLA (labeled with FITC) specifically bound to CXCR4 High . Cells were incubated with the peptide (5 μM) in 1.5% (w/v) FBS containing medium for 2h at 37°C prior to performing FACS analysis. (B) CXCR4-KLA displays the preferential cell killing of CXCR4 High compared to CXCR4 Low . MTS assays were performed on the cells 72 h after incubation with different concentrations (0–100 μM) of the peptide. (C) The specificity of CXCR4-KLA was confirmed by a reduction of the CXCR4 High fraction of both CXCR4 High and A2780/ADR after treatment with a suboptimal concentration (2 μM) of CXCR4-KLA for 72 h. (D) CXCR4-KLA is more potent than the conventional CXCR4 antagonists, including AMD3100 and CTCE9908, toward A2780, A2780/ADR, and SKOV3. Cells were incubated with the peptide (10 μM) for 72 h prior to determine the cell viability using MTS assay. (E) Using a combination of drugs (doxorubicin or cisplatin) and CXCR4-KLA (at suboptimal concentrations) showed synergistic cell-killing effects on CXCR4 High and CXCR4 Low (two way ANOVA, *** p
Figure Legend Snippet: CXCR4 High can be a useful target for OVC treatment. (A) CXCR4-KLA (labeled with FITC) specifically bound to CXCR4 High . Cells were incubated with the peptide (5 μM) in 1.5% (w/v) FBS containing medium for 2h at 37°C prior to performing FACS analysis. (B) CXCR4-KLA displays the preferential cell killing of CXCR4 High compared to CXCR4 Low . MTS assays were performed on the cells 72 h after incubation with different concentrations (0–100 μM) of the peptide. (C) The specificity of CXCR4-KLA was confirmed by a reduction of the CXCR4 High fraction of both CXCR4 High and A2780/ADR after treatment with a suboptimal concentration (2 μM) of CXCR4-KLA for 72 h. (D) CXCR4-KLA is more potent than the conventional CXCR4 antagonists, including AMD3100 and CTCE9908, toward A2780, A2780/ADR, and SKOV3. Cells were incubated with the peptide (10 μM) for 72 h prior to determine the cell viability using MTS assay. (E) Using a combination of drugs (doxorubicin or cisplatin) and CXCR4-KLA (at suboptimal concentrations) showed synergistic cell-killing effects on CXCR4 High and CXCR4 Low (two way ANOVA, *** p

Techniques Used: Labeling, Incubation, FACS, Concentration Assay, MTS Assay

9) Product Images from "Targeting the cancer-associated fibroblasts as a treatment in triple-negative breast cancer"

Article Title: Targeting the cancer-associated fibroblasts as a treatment in triple-negative breast cancer

Journal: Oncotarget

doi: 10.18632/oncotarget.12658

Pirfenidone inhibits primary tumor growth and lung metastasis in combination with doxorubicin in TNBC mouse model We transplanted 4T1 cells (1x10 4 ) and 4T1-stimulated CAFs (2x10 4 ) into mammary glands of BALB/c mice (n=5-6). PFD (50 mg/kg) or water was orally administered two times per day and doxorubicin (4 mg/kg) or PBS was injected from the mouse tail vain on day 0 and 19. A. Representative photographs of primary tumors after the treatments (Day 37) (left panel). Tumor volume (mm 3 ) was measured by “V=0.52xW 2 xL.” W=width (mm), L=length (mm). PFD had no effect on primary tumor growth, but inhibited the tumor growth synergistically in combination with doxorubicin. * p
Figure Legend Snippet: Pirfenidone inhibits primary tumor growth and lung metastasis in combination with doxorubicin in TNBC mouse model We transplanted 4T1 cells (1x10 4 ) and 4T1-stimulated CAFs (2x10 4 ) into mammary glands of BALB/c mice (n=5-6). PFD (50 mg/kg) or water was orally administered two times per day and doxorubicin (4 mg/kg) or PBS was injected from the mouse tail vain on day 0 and 19. A. Representative photographs of primary tumors after the treatments (Day 37) (left panel). Tumor volume (mm 3 ) was measured by “V=0.52xW 2 xL.” W=width (mm), L=length (mm). PFD had no effect on primary tumor growth, but inhibited the tumor growth synergistically in combination with doxorubicin. * p

Techniques Used: Mouse Assay, Injection

10) Product Images from "Focal therapy of neuroblastoma using silk films to deliver kinase and chemotherapeutic agents in vivo"

Article Title: Focal therapy of neuroblastoma using silk films to deliver kinase and chemotherapeutic agents in vivo

Journal: Acta biomaterialia

doi: 10.1016/j.actbio.2015.04.003

In vitro and in vivo response of doxorubicin-loaded silk films. (a) Long term toxicity of free doxorubicin and silk films loaded with doxorubicin. Culture medium was replaced at the indicated time. With the exception of control wells, wells were re-seeded
Figure Legend Snippet: In vitro and in vivo response of doxorubicin-loaded silk films. (a) Long term toxicity of free doxorubicin and silk films loaded with doxorubicin. Culture medium was replaced at the indicated time. With the exception of control wells, wells were re-seeded

Techniques Used: In Vitro, In Vivo

Characterization of silk films intended for local neuroblastoma therapy. ( a ) Conformity of silk films to tumor phantoms; ( b ) Weight and thickness of silk films in the dry and hydrated state; ( c ) Doxorubicin release kinetics from stabilized silk films;
Figure Legend Snippet: Characterization of silk films intended for local neuroblastoma therapy. ( a ) Conformity of silk films to tumor phantoms; ( b ) Weight and thickness of silk films in the dry and hydrated state; ( c ) Doxorubicin release kinetics from stabilized silk films;

Techniques Used:

11) Product Images from "Osteotropic therapy via targeted Layer-by-Layer nanoparticles"

Article Title: Osteotropic therapy via targeted Layer-by-Layer nanoparticles

Journal: Advanced healthcare materials

doi: 10.1002/adhm.201300465

in vitro evaluation of LbL-targeted liposomal NPs in 143B cells (A) Cryo-TEM of LbL-targeted doxorubicin-loaded liposomal NPs. Scale bar representative of 200 nm. (B) Binding (2 hour incubation) and relative cytotoxicity (48 hour incubation) of LbL-targeted empty liposomal NPs over a range of concentrations, based on fluorescence, in 143B cells (λ ex = 675 nm, λ em = 710 nm; tracked using PLL 700 as cationic component in LbL film). (C) Confocal microscopy of 143B cells incubated with the LbL-targeted empty liposomal NPs [tracked via PLL 700 polycationic component in LbL film] for 2 hours. Blue staining representative of a Hoescht nuclear stain, green representative of a phalloidin stain of the actin filamentous cell structure, and red representative of the nanoparticle fluorescence (PLL Cy5.5 polymer shell fluorescence). Scale bar representative of 10 μm. (D) Representative cell-associated NP fluorescence following a 2 hour incubation of 143B cells with the LbL-targeted empty liposomal NPs. (E) in vitro cytotoxicity of LbL-targeted doxorubicin-loaded liposomal NPs and the corresponding (F) uncoated doxorubicin-loaded liposomal control following 48 hour (blue) and 72 hour (red) incubation periods over a range of doxorubicin concentrations.
Figure Legend Snippet: in vitro evaluation of LbL-targeted liposomal NPs in 143B cells (A) Cryo-TEM of LbL-targeted doxorubicin-loaded liposomal NPs. Scale bar representative of 200 nm. (B) Binding (2 hour incubation) and relative cytotoxicity (48 hour incubation) of LbL-targeted empty liposomal NPs over a range of concentrations, based on fluorescence, in 143B cells (λ ex = 675 nm, λ em = 710 nm; tracked using PLL 700 as cationic component in LbL film). (C) Confocal microscopy of 143B cells incubated with the LbL-targeted empty liposomal NPs [tracked via PLL 700 polycationic component in LbL film] for 2 hours. Blue staining representative of a Hoescht nuclear stain, green representative of a phalloidin stain of the actin filamentous cell structure, and red representative of the nanoparticle fluorescence (PLL Cy5.5 polymer shell fluorescence). Scale bar representative of 10 μm. (D) Representative cell-associated NP fluorescence following a 2 hour incubation of 143B cells with the LbL-targeted empty liposomal NPs. (E) in vitro cytotoxicity of LbL-targeted doxorubicin-loaded liposomal NPs and the corresponding (F) uncoated doxorubicin-loaded liposomal control following 48 hour (blue) and 72 hour (red) incubation periods over a range of doxorubicin concentrations.

Techniques Used: In Vitro, Transmission Electron Microscopy, Binding Assay, Incubation, Fluorescence, Confocal Microscopy, Staining

143B xenograft tumor remediation following treatment with doxorubicin-loaded liposomal formulations (A) in vivo tumor remediation of 143B xenografts in NCR nude mice for LbL-targeted doxorubicin-loaded liposomal NPs, against untreated and uncoated doxorubicin-liposomal NPs. Untreated control xenografts were sacrificed 19 days post-inoculation of xenograft due to tumor burden exceeding 1 cm. Untargeted and targeted Dox-liposomal formulations were sacked at 30 days post-inoculation following a dose-escalation study with the following treatment regimen: day 10 at 1 mg/kg, day 17 at 2 mg/kg, day 24 at 3 mg/kg. Terminal point shown with final tumor area displayed in (B) . Statistics are from an unpaired t-test, two-tailed to compare the untargeted and targeted formulations at each time point. Data presented as mean +/− SEM; n = 4. (C) Caliper measurements for in vivo tumor remediation with repeated dosing of 5 mg/kg for both targeted and untargeted formulations at 22 days, 28 days, and 35 days post-inoculation (displayed as day 0, day 6, and day 13 in (C) ). Statistics are from an unpaired t-test, two-tailed to compare the untargeted and targeted formulations; *p
Figure Legend Snippet: 143B xenograft tumor remediation following treatment with doxorubicin-loaded liposomal formulations (A) in vivo tumor remediation of 143B xenografts in NCR nude mice for LbL-targeted doxorubicin-loaded liposomal NPs, against untreated and uncoated doxorubicin-liposomal NPs. Untreated control xenografts were sacrificed 19 days post-inoculation of xenograft due to tumor burden exceeding 1 cm. Untargeted and targeted Dox-liposomal formulations were sacked at 30 days post-inoculation following a dose-escalation study with the following treatment regimen: day 10 at 1 mg/kg, day 17 at 2 mg/kg, day 24 at 3 mg/kg. Terminal point shown with final tumor area displayed in (B) . Statistics are from an unpaired t-test, two-tailed to compare the untargeted and targeted formulations at each time point. Data presented as mean +/− SEM; n = 4. (C) Caliper measurements for in vivo tumor remediation with repeated dosing of 5 mg/kg for both targeted and untargeted formulations at 22 days, 28 days, and 35 days post-inoculation (displayed as day 0, day 6, and day 13 in (C) ). Statistics are from an unpaired t-test, two-tailed to compare the untargeted and targeted formulations; *p

Techniques Used: In Vivo, Mouse Assay, Two Tailed Test

12) Product Images from "Targeting uPAR by CRISPR/Cas9 System Attenuates Cancer Malignancy and Multidrug Resistance"

Article Title: Targeting uPAR by CRISPR/Cas9 System Attenuates Cancer Malignancy and Multidrug Resistance

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2019.00080

Knockout of uPAR decreases multidrug resistance. Cells survival was measured by MTT assay. The representative growth curve of HCT8/T (A) and KB V200 (B) cells treated with the indicated concentrations of 5-FU, cisplatin, docetaxel, and doxorubicin for 72 h were shown.
Figure Legend Snippet: Knockout of uPAR decreases multidrug resistance. Cells survival was measured by MTT assay. The representative growth curve of HCT8/T (A) and KB V200 (B) cells treated with the indicated concentrations of 5-FU, cisplatin, docetaxel, and doxorubicin for 72 h were shown.

Techniques Used: Knock-Out, MTT Assay

13) Product Images from "Trametinib modulates cancer multidrug resistance by targeting ABCB1 transporter"

Article Title: Trametinib modulates cancer multidrug resistance by targeting ABCB1 transporter

Journal: Oncotarget

doi:

Trametinib increases the intercellular accumulation of rhodamine 123 and doxorubicin in ABCB1-overexpressing cells Cells were incubated with 10μM rhodamin 123 or doxorubicin for another 2 hours at 37°C after pre-treated with the indicated concentrations of trametinib and verapemail for 1 hour at 37 °C, measured by FCM and photographed by fluorescent microscope. The representative charts ( A ), quantified data ( B ) and graphs ( C ) are shown. * P
Figure Legend Snippet: Trametinib increases the intercellular accumulation of rhodamine 123 and doxorubicin in ABCB1-overexpressing cells Cells were incubated with 10μM rhodamin 123 or doxorubicin for another 2 hours at 37°C after pre-treated with the indicated concentrations of trametinib and verapemail for 1 hour at 37 °C, measured by FCM and photographed by fluorescent microscope. The representative charts ( A ), quantified data ( B ) and graphs ( C ) are shown. * P

Techniques Used: Incubation, Microscopy

Trametinib in combination with ABCB1-substrate chemotherapeutic agents induces cell cycle arrest in the ABCB1-overexpressing cells Cells were treated with the indicated agents for 48 hours, and the distribution of cell cycle was detected by FCM with PI staining. The protein expression was examined by Western blot after lysing cells, and GAPDH was used as loading control. The concentrations of each agent were used as follow: vincristine 0.03 μM in KB and 0.3 μM in KB V200 , doxorubicin 0.01 μM in MCF-7 and 1 μM in MCF-7/ADR, trametinib 10 μM in all four cells. The representative charts ( A ), quantified data ( B ) and Western blot results ( C ) are shown. * P
Figure Legend Snippet: Trametinib in combination with ABCB1-substrate chemotherapeutic agents induces cell cycle arrest in the ABCB1-overexpressing cells Cells were treated with the indicated agents for 48 hours, and the distribution of cell cycle was detected by FCM with PI staining. The protein expression was examined by Western blot after lysing cells, and GAPDH was used as loading control. The concentrations of each agent were used as follow: vincristine 0.03 μM in KB and 0.3 μM in KB V200 , doxorubicin 0.01 μM in MCF-7 and 1 μM in MCF-7/ADR, trametinib 10 μM in all four cells. The representative charts ( A ), quantified data ( B ) and Western blot results ( C ) are shown. * P

Techniques Used: Staining, Expressing, Western Blot

Trametinib in combination with ABCB1-substrate chemotherapeutic agents induces apoptosis in the ABCB1-overexpressing cells Cells were treated with the indicated agents for 48 hours, and the apoptosis was detected by FCM Annexin V/PI staining. The proportions of Annexin V+/PI- and Annexin V+/PI+ cells indicated the early and late stage of apoptosis. The protein expression was examined by Western blot after lysing cells, and GAPDH was used as loading control. The concentrations of each agent were used as follow: vincristine 0.03 μM in KB and 0.3 μM in KB V200 , doxorubicin 0.01 μM in MCF-7 and 1 μM in MCF-7/ADR, trametinib 10 μM in all four cells. The representative charts ( A ), quantified data ( B ) and Western blot results ( C ) are shown. * P
Figure Legend Snippet: Trametinib in combination with ABCB1-substrate chemotherapeutic agents induces apoptosis in the ABCB1-overexpressing cells Cells were treated with the indicated agents for 48 hours, and the apoptosis was detected by FCM Annexin V/PI staining. The proportions of Annexin V+/PI- and Annexin V+/PI+ cells indicated the early and late stage of apoptosis. The protein expression was examined by Western blot after lysing cells, and GAPDH was used as loading control. The concentrations of each agent were used as follow: vincristine 0.03 μM in KB and 0.3 μM in KB V200 , doxorubicin 0.01 μM in MCF-7 and 1 μM in MCF-7/ADR, trametinib 10 μM in all four cells. The representative charts ( A ), quantified data ( B ) and Western blot results ( C ) are shown. * P

Techniques Used: Staining, Expressing, Western Blot

Trametinib enhances the sensitivity of ABCB1-substrate chemotherapeutic agents in the ABCB1-overexpressing cells Cells were treated with the indicated concentrations of trametinib ( A ) or other agents for 72 h, and cell survival was measured by MTT assay. The representative growth curve of KB, KB V200 , MCF-7 and MCF-7/ADR cells treated with trametinib alone ( B ) or in combination with vincristine, doxorubicin and cisplatin ( C ) are shown.
Figure Legend Snippet: Trametinib enhances the sensitivity of ABCB1-substrate chemotherapeutic agents in the ABCB1-overexpressing cells Cells were treated with the indicated concentrations of trametinib ( A ) or other agents for 72 h, and cell survival was measured by MTT assay. The representative growth curve of KB, KB V200 , MCF-7 and MCF-7/ADR cells treated with trametinib alone ( B ) or in combination with vincristine, doxorubicin and cisplatin ( C ) are shown.

Techniques Used: MTT Assay

14) Product Images from "Specific antioxidant compounds differentially modulate cytotoxic activity of doxorubicin and cisplatin: in vitro and in vivo study"

Article Title: Specific antioxidant compounds differentially modulate cytotoxic activity of doxorubicin and cisplatin: in vitro and in vivo study

Journal: Croatian Medical Journal

doi: 10.3325/cmj.2014.55.206

Sodium selenite, selenomethionine, and D-pantethine inhibit production of superoxide anions ( A ) and induction of apoptosis ( B ) in human breast adenocarcinoma cells of MCF-7 line under doxorubicin treatment. 1 – control; 2 – doxorubicin, 1 µM; 3 – doxorubicin, 1 µM+Na 2 SeO 3 , 0.1 µM; 4 – doxorubicin, 1 µM+selenomethionine, 0.1 µM; 5 – doxorubicin, 1 µM+D-pantethine, 25 µM.
Figure Legend Snippet: Sodium selenite, selenomethionine, and D-pantethine inhibit production of superoxide anions ( A ) and induction of apoptosis ( B ) in human breast adenocarcinoma cells of MCF-7 line under doxorubicin treatment. 1 – control; 2 – doxorubicin, 1 µM; 3 – doxorubicin, 1 µM+Na 2 SeO 3 , 0.1 µM; 4 – doxorubicin, 1 µM+selenomethionine, 0.1 µM; 5 – doxorubicin, 1 µM+D-pantethine, 25 µM.

Techniques Used:

Selenomethionine and D-pantethine restore content of coenzyme A-SH ( A ) and acetyl-coenzyme A ( B ) in the liver of normal rats after administration of doxorubicin. * P
Figure Legend Snippet: Selenomethionine and D-pantethine restore content of coenzyme A-SH ( A ) and acetyl-coenzyme A ( B ) in the liver of normal rats after administration of doxorubicin. * P

Techniques Used:

Sodium selenite, selenomethionine, and D-pantethine decrease cytotoxic action of doxorubicin toward human leukemia cells of Jurkat line and HL-60 line, but have no impact on doxorubicin action toward vincristin-resistant HL-60/vinc sub-line overexpressing P-glycoprotein. Medium – blank control (appropriate volume of culture medium added instead of antioxidants). * P
Figure Legend Snippet: Sodium selenite, selenomethionine, and D-pantethine decrease cytotoxic action of doxorubicin toward human leukemia cells of Jurkat line and HL-60 line, but have no impact on doxorubicin action toward vincristin-resistant HL-60/vinc sub-line overexpressing P-glycoprotein. Medium – blank control (appropriate volume of culture medium added instead of antioxidants). * P

Techniques Used:

D-pantethine, but not selenomethionine, restores the activity of succinate dehydrogenase (SDH) (nmol/mg protein* min) in the rat liver under doxorubicin treatment. * P
Figure Legend Snippet: D-pantethine, but not selenomethionine, restores the activity of succinate dehydrogenase (SDH) (nmol/mg protein* min) in the rat liver under doxorubicin treatment. * P

Techniques Used: Activity Assay

Sodium selenite, selenomethionine, and D-pantethine decrease cytotoxic action of doxorubicin toward wild-type HCT-116 cells, but have no impact on doxorubicin action toward HCT-116/Bax(−/−) and HCT-116/p53(−/−) sub-lines lacking Bax and p53 genes. Medium – blank control (appropriate volume of culture medium added instead of the antioxidants). * P
Figure Legend Snippet: Sodium selenite, selenomethionine, and D-pantethine decrease cytotoxic action of doxorubicin toward wild-type HCT-116 cells, but have no impact on doxorubicin action toward HCT-116/Bax(−/−) and HCT-116/p53(−/−) sub-lines lacking Bax and p53 genes. Medium – blank control (appropriate volume of culture medium added instead of the antioxidants). * P

Techniques Used:

15) Product Images from "Secreted Heat Shock Protein 90α Attenuated the Effect of Anticancer Drugs in Small-Cell Lung Cancer Cells Through AKT/GSK3β/β-Catenin Signaling"

Article Title: Secreted Heat Shock Protein 90α Attenuated the Effect of Anticancer Drugs in Small-Cell Lung Cancer Cells Through AKT/GSK3β/β-Catenin Signaling

Journal: Cancer Control : Journal of the Moffitt Cancer Center

doi: 10.1177/1073274818804489

Cell viabilities of (A) H69, (B) H82, and (C) H146 cells under the treatment of ABT-737 or doxorubicin. Enzyme-linked immunosorbent assay (ELISA) assay revealed the existence and concentrations of extracellular heat shock protein 90α (HSP 90α) in the medium of (D) H69, (E) H82, and (F) H146 cells under the treatment of ABT-737 or doxorubicin; (G) representative and (H) summary of Western blot assay for the existence and quantities of HSP 90α and β in culture medium of various cell types (as in eHSP90α and eHSP90β), and the amount of intracellular HSP 90α and β. * P
Figure Legend Snippet: Cell viabilities of (A) H69, (B) H82, and (C) H146 cells under the treatment of ABT-737 or doxorubicin. Enzyme-linked immunosorbent assay (ELISA) assay revealed the existence and concentrations of extracellular heat shock protein 90α (HSP 90α) in the medium of (D) H69, (E) H82, and (F) H146 cells under the treatment of ABT-737 or doxorubicin; (G) representative and (H) summary of Western blot assay for the existence and quantities of HSP 90α and β in culture medium of various cell types (as in eHSP90α and eHSP90β), and the amount of intracellular HSP 90α and β. * P

Techniques Used: Enzyme-linked Immunosorbent Assay, Western Blot

16) Product Images from "Hyaluronan Polymer Length, Grafting Density, and Surface Poly(ethylene glycol) Coating Influence in Vivo Circulation and Tumor Targeting of Hyaluronan-Grafted Liposomes"

Article Title: Hyaluronan Polymer Length, Grafting Density, and Surface Poly(ethylene glycol) Coating Influence in Vivo Circulation and Tumor Targeting of Hyaluronan-Grafted Liposomes

Journal: ACS Nano

doi: 10.1021/nn405839n

Ex vivo flow cytometry analysis of tumor cellular internalization of liposomes and cleaved caspase-3 staining after liposomal doxorubicin therapy. (A) Ex vivo tumor cellular internalization of DiD-labeled PEGylated liposomes and PEG-175–350kHA-liposomes. The tumor cells were harvested from disaggregated tumor. The internalized formulations were measured by flow cytometry, and mean fluorescence intensity was normalized to control (set as 100%). *Significant difference compared to PEGylated liposomes ( p
Figure Legend Snippet: Ex vivo flow cytometry analysis of tumor cellular internalization of liposomes and cleaved caspase-3 staining after liposomal doxorubicin therapy. (A) Ex vivo tumor cellular internalization of DiD-labeled PEGylated liposomes and PEG-175–350kHA-liposomes. The tumor cells were harvested from disaggregated tumor. The internalized formulations were measured by flow cytometry, and mean fluorescence intensity was normalized to control (set as 100%). *Significant difference compared to PEGylated liposomes ( p

Techniques Used: Ex Vivo, Flow Cytometry, Cytometry, Staining, Labeling, Fluorescence

17) Product Images from "Endoplasmic reticulum stress-mediated induction of SESTRIN 2 potentiates cell survival"

Article Title: Endoplasmic reticulum stress-mediated induction of SESTRIN 2 potentiates cell survival

Journal: Oncotarget

doi: 10.18632/oncotarget.7601

Chemotherapeutics, Methotrexate and Bortezomib, induce ER stress and SESTRIN 2 expression via UPR-mediated signals A.-B. HCC1806 (A) and MCF7 (B) cells were treated with 5 mM (A) 0.5 mM (B) 5-fluorouracil (5FU), 200 μM melphalan (Mel), 200 nM (A) 100 nM (B) Taxol, 20 μM Methotrexate (Mtx), 200 nM Doxorubicin, 0.5 μM Bortezomib (Btz) for 24 h and lysates immunoblotted for SESTRIN 2 and ACTIN. C. HCC1806 cells were treated with the indicated concentrations of Mtx for 48 h and lysates immunoblotted for SESTRIN 2, PERK, XBP1s, ATF4, CHOP and ACTIN. D. HCC1806 cells were treated with 20 μM Mtx for the indicated time and lysates immunoblotted for SESTRIN 2, LC3-I/II, XBP1s, ATF4, CHOP and ACTIN. E. HCC1806 cells were treated with 20 μM Mtx for the indicated time alone or in combination with 300 nM PERK or 10 μM IRE1 inhibitor and lysates were immunoblotted for SESTRIN 2, XBP1s and ACTIN. A representative image of 3 independent experiments is shown. F. Ctrl and XBP1 siRNA-transfected HCC1806 cells were treated with 20 μM Mtx for the indicated time and lysates immunoblotted for SESTRIN 2, XBP1s and ACTIN.
Figure Legend Snippet: Chemotherapeutics, Methotrexate and Bortezomib, induce ER stress and SESTRIN 2 expression via UPR-mediated signals A.-B. HCC1806 (A) and MCF7 (B) cells were treated with 5 mM (A) 0.5 mM (B) 5-fluorouracil (5FU), 200 μM melphalan (Mel), 200 nM (A) 100 nM (B) Taxol, 20 μM Methotrexate (Mtx), 200 nM Doxorubicin, 0.5 μM Bortezomib (Btz) for 24 h and lysates immunoblotted for SESTRIN 2 and ACTIN. C. HCC1806 cells were treated with the indicated concentrations of Mtx for 48 h and lysates immunoblotted for SESTRIN 2, PERK, XBP1s, ATF4, CHOP and ACTIN. D. HCC1806 cells were treated with 20 μM Mtx for the indicated time and lysates immunoblotted for SESTRIN 2, LC3-I/II, XBP1s, ATF4, CHOP and ACTIN. E. HCC1806 cells were treated with 20 μM Mtx for the indicated time alone or in combination with 300 nM PERK or 10 μM IRE1 inhibitor and lysates were immunoblotted for SESTRIN 2, XBP1s and ACTIN. A representative image of 3 independent experiments is shown. F. Ctrl and XBP1 siRNA-transfected HCC1806 cells were treated with 20 μM Mtx for the indicated time and lysates immunoblotted for SESTRIN 2, XBP1s and ACTIN.

Techniques Used: Expressing, Transfection

18) Product Images from "HSP-90 Inhibitor Ganetespib is Synergistic with Doxorubicin in Small Cell Lung Cancer"

Article Title: HSP-90 Inhibitor Ganetespib is Synergistic with Doxorubicin in Small Cell Lung Cancer

Journal: Oncogene

doi: 10.1038/onc.2013.439

A . TO-PRO-3 staining in H82 cells treated with 40 nM doxorubicin (Doxo), 30 nM ganetespib (Gane), 250nM etoposide (Etop), 40 nM Doxo + 30 nM Gane and 250 nM Etop + 30 nM Gane. TO-PRO-3 stain was performed at 24, 48, and 72 hours after drug treatment. Data summarize 3 independent experiments. P value was calculated by one-way ANOVA test. B. Synergy of doxorubicin + ganetespib or etoposide + ganetespib combinations was observed in GLC4 and H82 cells by MTS assay. Combination index (CI) was calculated using Calcusyn algorithm (see Materials and Methods). CI of
Figure Legend Snippet: A . TO-PRO-3 staining in H82 cells treated with 40 nM doxorubicin (Doxo), 30 nM ganetespib (Gane), 250nM etoposide (Etop), 40 nM Doxo + 30 nM Gane and 250 nM Etop + 30 nM Gane. TO-PRO-3 stain was performed at 24, 48, and 72 hours after drug treatment. Data summarize 3 independent experiments. P value was calculated by one-way ANOVA test. B. Synergy of doxorubicin + ganetespib or etoposide + ganetespib combinations was observed in GLC4 and H82 cells by MTS assay. Combination index (CI) was calculated using Calcusyn algorithm (see Materials and Methods). CI of

Techniques Used: Staining, MTS Assay

A. Western blot analysis of H82 and GLC4 cells treated with the indicated drugs after 24h and 48h exposure . B. Western blot analysis of H82 and GLC4 cells transfected with 10nM or 15nM of control or RIP1 siRNAs for 72 hrs. C. TUNEL staining of H82 cells 72 hrs after the following treatment: a. Negative control siRNA; b. Doxorubicin (40nM); c. RIP1 siRNA (5nM); d. Doxorubicin (40nM) and RIP1 (5nM) siRNA combination. Note that lipofectamine was added in doxorubicin treatment group as a transfection reagent control. 400X magnification. D. Quantification of TUNEL staining in H82 and GLC4 cells. Each column represents means ± SD of at least three independent experiments. The columns are: 1. 0.2% Lipofectamine 72 hours; 2. Control siRNA 5nM (H82), 10nM (GLC4) 72 hours; 3. RIP1 siRNA 5nM (H82), 10nM (GLC4) 72 hours; 4. 0.2% Lipofectamine 72 hours plus doxorubicin 40nM 48 hours; 5. RIP1 siRNA 5nM (H82), 10nM (GLC4) 72 hours plus doxorubicin 40nM 48 hours . E. Percentage of viable H82 and GLC4 cells. Bars indicate standard errors. Column numbers are the same as in D.
Figure Legend Snippet: A. Western blot analysis of H82 and GLC4 cells treated with the indicated drugs after 24h and 48h exposure . B. Western blot analysis of H82 and GLC4 cells transfected with 10nM or 15nM of control or RIP1 siRNAs for 72 hrs. C. TUNEL staining of H82 cells 72 hrs after the following treatment: a. Negative control siRNA; b. Doxorubicin (40nM); c. RIP1 siRNA (5nM); d. Doxorubicin (40nM) and RIP1 (5nM) siRNA combination. Note that lipofectamine was added in doxorubicin treatment group as a transfection reagent control. 400X magnification. D. Quantification of TUNEL staining in H82 and GLC4 cells. Each column represents means ± SD of at least three independent experiments. The columns are: 1. 0.2% Lipofectamine 72 hours; 2. Control siRNA 5nM (H82), 10nM (GLC4) 72 hours; 3. RIP1 siRNA 5nM (H82), 10nM (GLC4) 72 hours; 4. 0.2% Lipofectamine 72 hours plus doxorubicin 40nM 48 hours; 5. RIP1 siRNA 5nM (H82), 10nM (GLC4) 72 hours plus doxorubicin 40nM 48 hours . E. Percentage of viable H82 and GLC4 cells. Bars indicate standard errors. Column numbers are the same as in D.

Techniques Used: Western Blot, Transfection, TUNEL Assay, Staining, Negative Control

A. Mouse xenograft study of H82 cells. p-value was calculated by one-way ANOVA at day 20 after drug treatment. p values were significant between any two group comparisons except for the doxorubicin and ganetespib comparison. %T/C value was calculated at the end of the experiment according to the following formula: ( Δ treated tumor volume / Δ control tumor volume ) × 100 , where Δtumor volume represents the mean tumor volume on the evaluation day minus the mean tumor volume at the start of the experiment. Bars indicate standard errors. Drug doses and schedules are indicated in the graph. B. Western blot analysis of H82 xenograft tumors harvested at the end of drug treatment experiments. C. H E stain of H82 xenograft tumors. a. Vehicle; b. Doxorubicin 4mg/kg treated every other day; c. Ganetespib 150mg/kg treated every week; d. Combination treatment. * Necrosis; 200X. Quantitations of necrosis (% area on H E stained slides) by a pathologist (M.R.) are shown on the right.
Figure Legend Snippet: A. Mouse xenograft study of H82 cells. p-value was calculated by one-way ANOVA at day 20 after drug treatment. p values were significant between any two group comparisons except for the doxorubicin and ganetespib comparison. %T/C value was calculated at the end of the experiment according to the following formula: ( Δ treated tumor volume / Δ control tumor volume ) × 100 , where Δtumor volume represents the mean tumor volume on the evaluation day minus the mean tumor volume at the start of the experiment. Bars indicate standard errors. Drug doses and schedules are indicated in the graph. B. Western blot analysis of H82 xenograft tumors harvested at the end of drug treatment experiments. C. H E stain of H82 xenograft tumors. a. Vehicle; b. Doxorubicin 4mg/kg treated every other day; c. Ganetespib 150mg/kg treated every week; d. Combination treatment. * Necrosis; 200X. Quantitations of necrosis (% area on H E stained slides) by a pathologist (M.R.) are shown on the right.

Techniques Used: Western Blot, Staining

19) Product Images from "Secreted Heat Shock Protein 90α Attenuated the Effect of Anticancer Drugs in Small-Cell Lung Cancer Cells Through AKT/GSK3β/β-Catenin Signaling"

Article Title: Secreted Heat Shock Protein 90α Attenuated the Effect of Anticancer Drugs in Small-Cell Lung Cancer Cells Through AKT/GSK3β/β-Catenin Signaling

Journal: Cancer Control : Journal of the Moffitt Cancer Center

doi: 10.1177/1073274818804489

Cell viabilities of (A) H69, (B) H82, and (C) H146 cells under the treatment of ABT-737 or doxorubicin. Enzyme-linked immunosorbent assay (ELISA) assay revealed the existence and concentrations of extracellular heat shock protein 90α (HSP 90α) in the medium of (D) H69, (E) H82, and (F) H146 cells under the treatment of ABT-737 or doxorubicin; (G) representative and (H) summary of Western blot assay for the existence and quantities of HSP 90α and β in culture medium of various cell types (as in eHSP90α and eHSP90β), and the amount of intracellular HSP 90α and β. * P
Figure Legend Snippet: Cell viabilities of (A) H69, (B) H82, and (C) H146 cells under the treatment of ABT-737 or doxorubicin. Enzyme-linked immunosorbent assay (ELISA) assay revealed the existence and concentrations of extracellular heat shock protein 90α (HSP 90α) in the medium of (D) H69, (E) H82, and (F) H146 cells under the treatment of ABT-737 or doxorubicin; (G) representative and (H) summary of Western blot assay for the existence and quantities of HSP 90α and β in culture medium of various cell types (as in eHSP90α and eHSP90β), and the amount of intracellular HSP 90α and β. * P

Techniques Used: Enzyme-linked Immunosorbent Assay, Western Blot

20) Product Images from "Biomimetic microfluidic platform for the quantification of transient endothelial monolayer permeability and therapeutic transport under mimicked cancerous conditions"

Article Title: Biomimetic microfluidic platform for the quantification of transient endothelial monolayer permeability and therapeutic transport under mimicked cancerous conditions

Journal: Biomicrofluidics

doi: 10.1063/1.5000377

Normalized percentage of BAOEC monolayer permeability under various culturing conditions. Data shown as a sum of means ± S.D. (n = 5 independent microfluidic devices) for each image collection method. (a) Percentage of confluent BAOEC monolayer intact without HCT116s, with HCT116s, after treatment with Paclitaxel, and after treatment with Doxorubicin for 24 h, measured as a percentage of the entire imaging field, collected via standard fluorescent microscopy. One way analysis of variance (one-way ANOVA) statistical analysis with statistical significance indicated by * brackets in plot at p ≤ 0.05. Sample collection was carried out from 5 independent devices (biological replicates). All statistical tests have been justified as appropriate. (b) Percentage of intercellular gap coverage without HCT116s, with HCT116s, after treatment with Paclitaxel, and after treatment with Doxorubicin, measured as a percentage of the entire imaging field, collected via fluorescent confocal microscopy. One way ANOVA statistical analysis with statistical significance indicated by * brackets in plot at p ≤ 0.05. Sample collection was carried out from 5 independent devices (biological replicates). All statistical tests have been justified as appropriate. (c) Representative fluorescent image of the highly confluent BAOEC monolayer prior to introduction of HCT116s into the device. Cells in the image were stained with Cell Tracker Green and the red arrow indicates the direction of flow within the channel. ( d) Representative fluorescent image of the permeabilized BAOEC monolayer after introduction of HCT116s into the device. Cells in image were stained with Cell Tracker Green and the red arrow indicates the direction of flow within the channel. Both red scale bars are 50 μ m in length.
Figure Legend Snippet: Normalized percentage of BAOEC monolayer permeability under various culturing conditions. Data shown as a sum of means ± S.D. (n = 5 independent microfluidic devices) for each image collection method. (a) Percentage of confluent BAOEC monolayer intact without HCT116s, with HCT116s, after treatment with Paclitaxel, and after treatment with Doxorubicin for 24 h, measured as a percentage of the entire imaging field, collected via standard fluorescent microscopy. One way analysis of variance (one-way ANOVA) statistical analysis with statistical significance indicated by * brackets in plot at p ≤ 0.05. Sample collection was carried out from 5 independent devices (biological replicates). All statistical tests have been justified as appropriate. (b) Percentage of intercellular gap coverage without HCT116s, with HCT116s, after treatment with Paclitaxel, and after treatment with Doxorubicin, measured as a percentage of the entire imaging field, collected via fluorescent confocal microscopy. One way ANOVA statistical analysis with statistical significance indicated by * brackets in plot at p ≤ 0.05. Sample collection was carried out from 5 independent devices (biological replicates). All statistical tests have been justified as appropriate. (c) Representative fluorescent image of the highly confluent BAOEC monolayer prior to introduction of HCT116s into the device. Cells in the image were stained with Cell Tracker Green and the red arrow indicates the direction of flow within the channel. ( d) Representative fluorescent image of the permeabilized BAOEC monolayer after introduction of HCT116s into the device. Cells in image were stained with Cell Tracker Green and the red arrow indicates the direction of flow within the channel. Both red scale bars are 50 μ m in length.

Techniques Used: Permeability, Imaging, Microscopy, Confocal Microscopy, Staining, Flow Cytometry

21) Product Images from "Chemotherapy-Induced Tunneling Nanotubes Mediate Intercellular Drug Efflux in Pancreatic Cancer"

Article Title: Chemotherapy-Induced Tunneling Nanotubes Mediate Intercellular Drug Efflux in Pancreatic Cancer

Journal: Scientific Reports

doi: 10.1038/s41598-018-27649-x

Variable dose-dependent response of TNTs forming after exposure to the chemotherapeutic drug doxorubicin. ( A ) Representative images of TNTs transmitting autofluorescing (red) doxorubicin between S2013 cells. Images were taken using a Zeiss Axio widefield microscope. Scale bars = 50 μm. ( B , C ) Scatter-plot graph depicting the median number of TNTs/cell (TNT index) over time, comparing results for the S2013 (Panel B) and MIA PaCa-2 (Panel C) cell lines after exposure to six concentrations of doxorubicin. This experiment was done in triplicate, with a sample size of 18 fields of view per dose/per time point.
Figure Legend Snippet: Variable dose-dependent response of TNTs forming after exposure to the chemotherapeutic drug doxorubicin. ( A ) Representative images of TNTs transmitting autofluorescing (red) doxorubicin between S2013 cells. Images were taken using a Zeiss Axio widefield microscope. Scale bars = 50 μm. ( B , C ) Scatter-plot graph depicting the median number of TNTs/cell (TNT index) over time, comparing results for the S2013 (Panel B) and MIA PaCa-2 (Panel C) cell lines after exposure to six concentrations of doxorubicin. This experiment was done in triplicate, with a sample size of 18 fields of view per dose/per time point.

Techniques Used: Microscopy

TNTs act as a direct conduit for intercellular transfer and redistribution of the chemotherapeutic drug doxorubicin. ( A ) TNT formation and intercellular transfer of doxorubicin between S2013 pancreatic adenocarcinoma cells. ( B ) Composite of serial images from time-lapse microscopy demonstrating intercellular transfer of doxorubicin from a chemoresistant ovarian cancer cell (SKOV3) to a chemosensitive cell (A2780) via a TNT, resulting in cell death of the chemosensitive cell. Images were taken every 15 minutes for 24 hours using a wide-field Zeiss Axio200M microscope.
Figure Legend Snippet: TNTs act as a direct conduit for intercellular transfer and redistribution of the chemotherapeutic drug doxorubicin. ( A ) TNT formation and intercellular transfer of doxorubicin between S2013 pancreatic adenocarcinoma cells. ( B ) Composite of serial images from time-lapse microscopy demonstrating intercellular transfer of doxorubicin from a chemoresistant ovarian cancer cell (SKOV3) to a chemosensitive cell (A2780) via a TNT, resulting in cell death of the chemosensitive cell. Images were taken every 15 minutes for 24 hours using a wide-field Zeiss Axio200M microscope.

Techniques Used: Activated Clotting Time Assay, Time-lapse Microscopy, Microscopy

22) Product Images from "Trojan Horse nanotheranostics with dual transformability and multifunctionality for highly effective cancer treatment"

Article Title: Trojan Horse nanotheranostics with dual transformability and multifunctionality for highly effective cancer treatment

Journal: Nature Communications

doi: 10.1038/s41467-018-06093-5

Schematic illustration of the Trojan-Horse nanoparticles. Image illustration of the functionalities of the building blocks and construction of the Trojan-Horse nanoparticles (pPhD NPs), and their capabilities to overcome a series of biological barriers through TME responsiveness, de-PEGylation/cross-linkage, transformability, superior penetrations, enhanced cell internalisation, intracellular drug release for multimodal imaging and trimodality therapies. Abbreviations: PDT photodynamic therapy, PTT photothermal therapy, NIRFI near-infrared fluorescence imaging, MRI magnetic resonance imaging, TME tumour microenvironment, Red square denotes Phy, and blue circle denotes DOX, PhD pheophorbide a-hydrazone-doxorubicin, upPhD NPs unPEGylated PhD NPs, pPhD NPs PEGylated PhD NPs, 1 O 2 reactive oxygen species
Figure Legend Snippet: Schematic illustration of the Trojan-Horse nanoparticles. Image illustration of the functionalities of the building blocks and construction of the Trojan-Horse nanoparticles (pPhD NPs), and their capabilities to overcome a series of biological barriers through TME responsiveness, de-PEGylation/cross-linkage, transformability, superior penetrations, enhanced cell internalisation, intracellular drug release for multimodal imaging and trimodality therapies. Abbreviations: PDT photodynamic therapy, PTT photothermal therapy, NIRFI near-infrared fluorescence imaging, MRI magnetic resonance imaging, TME tumour microenvironment, Red square denotes Phy, and blue circle denotes DOX, PhD pheophorbide a-hydrazone-doxorubicin, upPhD NPs unPEGylated PhD NPs, pPhD NPs PEGylated PhD NPs, 1 O 2 reactive oxygen species

Techniques Used: Imaging, Fluorescence, Magnetic Resonance Imaging

23) Product Images from "Pro-apoptotic Chemotherapeutic Drugs Induce Non-canonical Processing and Release of IL-1β via Caspase-8 in Dendritic Cells"

Article Title: Pro-apoptotic Chemotherapeutic Drugs Induce Non-canonical Processing and Release of IL-1β via Caspase-8 in Dendritic Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1300645

Doxorubicin induces caspase-1 independent processing and release of IL-1β in LPS-primed BMDC
Figure Legend Snippet: Doxorubicin induces caspase-1 independent processing and release of IL-1β in LPS-primed BMDC

Techniques Used:

Doxorubicin induces caspase-8 dependent IL-1β processing and release in LPS-primed BMDC
Figure Legend Snippet: Doxorubicin induces caspase-8 dependent IL-1β processing and release in LPS-primed BMDC

Techniques Used:

24) Product Images from "Wallichinine reverses ABCB1-mediated cancer multidrug resistance"

Article Title: Wallichinine reverses ABCB1-mediated cancer multidrug resistance

Journal: American Journal of Translational Research

doi:

Wallichinine increases the intercellular accumulation of rhodamine 123 and doxorubicin in ABCB1-overexpressing cells. Cells were incubated with 10 μM rhodamine 123 or doxorubicin for another 2 hours at 37°C after pre-treated with 10 μM
Figure Legend Snippet: Wallichinine increases the intercellular accumulation of rhodamine 123 and doxorubicin in ABCB1-overexpressing cells. Cells were incubated with 10 μM rhodamine 123 or doxorubicin for another 2 hours at 37°C after pre-treated with 10 μM

Techniques Used: Incubation

25) Product Images from "Combined Effect of Anticancer Agents and Cytochrome C Decorated Hybrid Nanoparticles for Liver Cancer Therapy"

Article Title: Combined Effect of Anticancer Agents and Cytochrome C Decorated Hybrid Nanoparticles for Liver Cancer Therapy

Journal: Pharmaceutics

doi: 10.3390/pharmaceutics10020048

Cell viability measured using the MTT assay of ( A ) doxorubicin, ( B ) paclitaxel, ( C ) oxaliplatin, ( D ) vinblastine and ( E ) vincristine as a single therapy and in combination with HNP-c after 48 h incubation in HepG2, Huh-7D and SK-hep-1 cell lines ( n = 3, ±SD). * denotes significant decrease in IC 50 compared to single drug treatment ( p
Figure Legend Snippet: Cell viability measured using the MTT assay of ( A ) doxorubicin, ( B ) paclitaxel, ( C ) oxaliplatin, ( D ) vinblastine and ( E ) vincristine as a single therapy and in combination with HNP-c after 48 h incubation in HepG2, Huh-7D and SK-hep-1 cell lines ( n = 3, ±SD). * denotes significant decrease in IC 50 compared to single drug treatment ( p

Techniques Used: MTT Assay, Incubation

26) Product Images from "Bioengineered NRF2-siRNA Is Effective to Interfere with NRF2 Pathways and Improve Chemosensitivity of Human Cancer Cells"

Article Title: Bioengineered NRF2-siRNA Is Effective to Interfere with NRF2 Pathways and Improve Chemosensitivity of Human Cancer Cells

Journal: Drug Metabolism and Disposition

doi: 10.1124/dmd.117.078741

BERA/NRF2-siRNA improves the chemosensitivity of human OS cells. BERA/NRF2-siRNA (2 nM) significantly sensitized 143B and MG63 cells to doxorubicin (A), cisplatin (B), and sorafenib (C), respectively (values are the mean ± S.D. of triplicate treatments; two-way ANOVA with Bonferroni post-hoc tests: P
Figure Legend Snippet: BERA/NRF2-siRNA improves the chemosensitivity of human OS cells. BERA/NRF2-siRNA (2 nM) significantly sensitized 143B and MG63 cells to doxorubicin (A), cisplatin (B), and sorafenib (C), respectively (values are the mean ± S.D. of triplicate treatments; two-way ANOVA with Bonferroni post-hoc tests: P

Techniques Used:

27) Product Images from "Doxorubicin-loaded silk films: drug-silk interactions and in vivo performance in human orthotopic breast cancer"

Article Title: Doxorubicin-loaded silk films: drug-silk interactions and in vivo performance in human orthotopic breast cancer

Journal: Biomaterials

doi: 10.1016/j.biomaterials.2012.08.004

Doxorubicin interactions and film stability. (A) Typical adsorption kinetics of doxorubicin to silk monitored by following doxorubicin depletion from solution using UV-Vis spectroscopy. (B) Equilibrium binding studies of doxorubicin to silk films. Graph
Figure Legend Snippet: Doxorubicin interactions and film stability. (A) Typical adsorption kinetics of doxorubicin to silk monitored by following doxorubicin depletion from solution using UV-Vis spectroscopy. (B) Equilibrium binding studies of doxorubicin to silk films. Graph

Techniques Used: Adsorption, UV-Vis Spectroscopy, Binding Assay

In vivo toxicity following systemic and local doxorubicin application. (A) Image depicting tumour and stabilised silk film at the time of necroscopy (week 6, scale bar 5 mm). (B) Heart weights of animals treated with localised or systemic doxorubicin
Figure Legend Snippet: In vivo toxicity following systemic and local doxorubicin application. (A) Image depicting tumour and stabilised silk film at the time of necroscopy (week 6, scale bar 5 mm). (B) Heart weights of animals treated with localised or systemic doxorubicin

Techniques Used: In Vivo

Preparation of doxorubicin-loaded silk films. (A) Strategies to generate doxorubicin-loaded films that are water-soluble or (B) water-insoluble with variable β-sheet content. (C) Film thickness of dry and hydrated silk films (± SD; n =
Figure Legend Snippet: Preparation of doxorubicin-loaded silk films. (A) Strategies to generate doxorubicin-loaded films that are water-soluble or (B) water-insoluble with variable β-sheet content. (C) Film thickness of dry and hydrated silk films (± SD; n =

Techniques Used:

In vitro toxicity of doxorubicin-loaded silk films towards human breast cancer cells. (A) MDA-MB-231 cell viability following a 72-h exposure to soluble or stabilised silk films ± doxorubicin and freely diffusible doxorubicin at the equivalent
Figure Legend Snippet: In vitro toxicity of doxorubicin-loaded silk films towards human breast cancer cells. (A) MDA-MB-231 cell viability following a 72-h exposure to soluble or stabilised silk films ± doxorubicin and freely diffusible doxorubicin at the equivalent

Techniques Used: In Vitro, Multiple Displacement Amplification

In vivo response of orthotopic breast tumours to doxorubicin-loaded silk films. (A) Cancer cell-associated bioluminescence at week 3, (B) 5 and (C) 6 weeks. (D) Weight of primary tumours at the end of the study (week 6). (E) In vivo tumour cell-specific
Figure Legend Snippet: In vivo response of orthotopic breast tumours to doxorubicin-loaded silk films. (A) Cancer cell-associated bioluminescence at week 3, (B) 5 and (C) 6 weeks. (D) Weight of primary tumours at the end of the study (week 6). (E) In vivo tumour cell-specific

Techniques Used: In Vivo

28) Product Images from "The anticancer natural product ophiobolin A induces cytotoxicity by covalent modification of phosphatidylethanolamine"

Article Title: The anticancer natural product ophiobolin A induces cytotoxicity by covalent modification of phosphatidylethanolamine

Journal: eLife

doi: 10.7554/eLife.14601

Validation of KBM7 loss-of-function screens using anticancer drugs with well-characterized mechanisms of action. ( a–f ) Loss-of-function genetic screens were performed and displayed as described in Figure 1a . Cells were treated with anticancer drugs at the concentration specified in each panel. Green bubbles represent genes known to be involved in the mechanism of action of the drug tested and the diameter of the bubble is proportional to the number of unique insertion sites in the pooled resistant clones (doxorubicin, TOP2A : N = 4; etoposide, TOP2A : N = 5; topotecan, TOP1 : N = 10; bortezomib, PSMC6 : N = 8; oxaliplatin, SLC43A2 : N = 5; gemcitabine, DCK : N = 161). Genes with a total of less than 50 sequencing reads were not displayed in the bubble plots. ( a ) The screen with doxorubicin uncovered TOP2A , which encodes topoisomerase IIA, the direct target of doxorubicin ( Tewey et al., 1984 ). ( b ) The screen with etoposide uncovered TOP2A , consistent with its known mechanism of action ( Montecucco and Biamonti, 2007 ). ( c ) The screen with topotecan identified its known direct target ( Pommier, 2006 ), type I topoisomerase (TOP1), as well as ABCG2 . It is known that overexpression, not inactivation, of this transporter causes resistance to topotecan ( Mao and Unadkat, 2015 ). In the pooled resistant clones, retroviral integration sites clustered to the beginning of the ABCG2 transcript and most were actually found upstream of the transcription start site (TSS). A topotecan-resistant clone (ABCG2 GT ) with a retroviral site 400 bp upstream of the TSS of ABCG2 was isolated and the expression level of ABCG2 was determined by RT-qPCR (Materials and methods). ABCG2 GT displayed a △△C T of 6.2 ± 0.3 compared to KBM7 indicating an increase in ABCG2 mRNA levels of up to 70-fold compared to KBM7 (mean values of three independent experiments ± standard deviation). ( d ) The screen with bortezomib, a proteasome inhibitor ( Adams, 2004 ), identified proteasome subunits ( PSMC6 , PSMD12 , PSMC5 , PSMD7 , PSMD2 ). ( e ) The screen with oxaliplatin, a DNA crosslinker, identified SLC43A2 , a solute carrier that transports neutral amino acids into cells ( Bodoy et al., 2013 ), suggesting that SLC43A2 facilitates the transport of oxaliplatin into cells consistent with the known role of solute carriers in the transport of anticancer drugs ( Li and Shu, 2014 ). ( f ) The screen with gemcitabine, a deoxycytidine analog, identified DCK and CDADC1 . Deficiency of DCK is associated with gemcitabine resistance ( Bergman et al., 2002 ) and CDADC1 is a cytidine and dCMP deaminase known to be involved in resistance to deoxycytidine analogs ( Cai et al., 2008 ) ( Figure 1—figure supplement 2—source data 1 ). DOI: http://dx.doi.org/10.7554/eLife.14601.007 10.7554/eLife.14601.008 Source data for anticancer drug loss-of-function KBM7 screens. DOI: http://dx.doi.org/10.7554/eLife.14601.008
Figure Legend Snippet: Validation of KBM7 loss-of-function screens using anticancer drugs with well-characterized mechanisms of action. ( a–f ) Loss-of-function genetic screens were performed and displayed as described in Figure 1a . Cells were treated with anticancer drugs at the concentration specified in each panel. Green bubbles represent genes known to be involved in the mechanism of action of the drug tested and the diameter of the bubble is proportional to the number of unique insertion sites in the pooled resistant clones (doxorubicin, TOP2A : N = 4; etoposide, TOP2A : N = 5; topotecan, TOP1 : N = 10; bortezomib, PSMC6 : N = 8; oxaliplatin, SLC43A2 : N = 5; gemcitabine, DCK : N = 161). Genes with a total of less than 50 sequencing reads were not displayed in the bubble plots. ( a ) The screen with doxorubicin uncovered TOP2A , which encodes topoisomerase IIA, the direct target of doxorubicin ( Tewey et al., 1984 ). ( b ) The screen with etoposide uncovered TOP2A , consistent with its known mechanism of action ( Montecucco and Biamonti, 2007 ). ( c ) The screen with topotecan identified its known direct target ( Pommier, 2006 ), type I topoisomerase (TOP1), as well as ABCG2 . It is known that overexpression, not inactivation, of this transporter causes resistance to topotecan ( Mao and Unadkat, 2015 ). In the pooled resistant clones, retroviral integration sites clustered to the beginning of the ABCG2 transcript and most were actually found upstream of the transcription start site (TSS). A topotecan-resistant clone (ABCG2 GT ) with a retroviral site 400 bp upstream of the TSS of ABCG2 was isolated and the expression level of ABCG2 was determined by RT-qPCR (Materials and methods). ABCG2 GT displayed a △△C T of 6.2 ± 0.3 compared to KBM7 indicating an increase in ABCG2 mRNA levels of up to 70-fold compared to KBM7 (mean values of three independent experiments ± standard deviation). ( d ) The screen with bortezomib, a proteasome inhibitor ( Adams, 2004 ), identified proteasome subunits ( PSMC6 , PSMD12 , PSMC5 , PSMD7 , PSMD2 ). ( e ) The screen with oxaliplatin, a DNA crosslinker, identified SLC43A2 , a solute carrier that transports neutral amino acids into cells ( Bodoy et al., 2013 ), suggesting that SLC43A2 facilitates the transport of oxaliplatin into cells consistent with the known role of solute carriers in the transport of anticancer drugs ( Li and Shu, 2014 ). ( f ) The screen with gemcitabine, a deoxycytidine analog, identified DCK and CDADC1 . Deficiency of DCK is associated with gemcitabine resistance ( Bergman et al., 2002 ) and CDADC1 is a cytidine and dCMP deaminase known to be involved in resistance to deoxycytidine analogs ( Cai et al., 2008 ) ( Figure 1—figure supplement 2—source data 1 ). DOI: http://dx.doi.org/10.7554/eLife.14601.007 10.7554/eLife.14601.008 Source data for anticancer drug loss-of-function KBM7 screens. DOI: http://dx.doi.org/10.7554/eLife.14601.008

Techniques Used: Concentration Assay, Clone Assay, Sequencing, Over Expression, Isolation, Expressing, Quantitative RT-PCR, Standard Deviation

29) Product Images from "Molecular-guided therapy predictions reveal drug resistance phenotypes and treatment alternatives in malignant peripheral nerve sheath tumors"

Article Title: Molecular-guided therapy predictions reveal drug resistance phenotypes and treatment alternatives in malignant peripheral nerve sheath tumors

Journal: Journal of Translational Medicine

doi: 10.1186/1479-5876-11-213

Doxorubicin-mediated growth inhibition in MPNST-derived NF02.2 cells with high ABCC1 expression. A) Relative cell content (as a percentage of untreated control cells) following 96 hours of growth in doxorubicin-containing media with and without 100 μM verapamil. Average doxorubicin EC 50 1.23 μg/ml, versus 0.21 μg/ml in the presence of verapamil *p = 0.003, n = 5. B) No growth inhibition is observed with verapamil alone at concentrations 125 μM and lower. Dotted line indicates 100 μM concentration used in (A) .
Figure Legend Snippet: Doxorubicin-mediated growth inhibition in MPNST-derived NF02.2 cells with high ABCC1 expression. A) Relative cell content (as a percentage of untreated control cells) following 96 hours of growth in doxorubicin-containing media with and without 100 μM verapamil. Average doxorubicin EC 50 1.23 μg/ml, versus 0.21 μg/ml in the presence of verapamil *p = 0.003, n = 5. B) No growth inhibition is observed with verapamil alone at concentrations 125 μM and lower. Dotted line indicates 100 μM concentration used in (A) .

Techniques Used: Inhibition, Derivative Assay, Expressing, Concentration Assay

ABCC1 expression and transporter function in MPNST-derived cell lines NF94.3 and NF96.2. Immunofluorescent staining for ABCC1 (green) and S100 (red) with DAPI (blue) nuclear stain as indicated in NF94.3 (A) and NF96.2 (B) . Scale bar = 10 μm. C) Relative cell content following 5 days of growth in doxorubicin-containing media with and without 100 μM verapamil in NF94.3 cells. Average doxorubicin EC 50 0.81 μg/ml, versus 0.34 μg/ml in the presence of verapamil (*p = 0.025, n = 5). D) NF96.2 cells; average doxorubicin EC 50 0.44 μg/ml, versus 0.22 μg/ml in the presence of verapamil (n.s. p = 0.16, n = 5). E) No growth inhibition with verapamil alone at concentrations 125 μM and lower. Dotted line indicates 100 μM verapamil concentration used in (C, D) . F) Quantitative real-time PCR for ABCC family transporter transcript levels. G) Doxorubicin EC 50 values for benign neurofibroma-derived cell lines as compared to MPNST-derived cell lines. H) Growth inhibition curves for a representative experiment with molecular-guided therapy predicted drugs. Data is graphed as percentage untreated control per drug concentration.
Figure Legend Snippet: ABCC1 expression and transporter function in MPNST-derived cell lines NF94.3 and NF96.2. Immunofluorescent staining for ABCC1 (green) and S100 (red) with DAPI (blue) nuclear stain as indicated in NF94.3 (A) and NF96.2 (B) . Scale bar = 10 μm. C) Relative cell content following 5 days of growth in doxorubicin-containing media with and without 100 μM verapamil in NF94.3 cells. Average doxorubicin EC 50 0.81 μg/ml, versus 0.34 μg/ml in the presence of verapamil (*p = 0.025, n = 5). D) NF96.2 cells; average doxorubicin EC 50 0.44 μg/ml, versus 0.22 μg/ml in the presence of verapamil (n.s. p = 0.16, n = 5). E) No growth inhibition with verapamil alone at concentrations 125 μM and lower. Dotted line indicates 100 μM verapamil concentration used in (C, D) . F) Quantitative real-time PCR for ABCC family transporter transcript levels. G) Doxorubicin EC 50 values for benign neurofibroma-derived cell lines as compared to MPNST-derived cell lines. H) Growth inhibition curves for a representative experiment with molecular-guided therapy predicted drugs. Data is graphed as percentage untreated control per drug concentration.

Techniques Used: Expressing, Derivative Assay, Staining, Inhibition, Concentration Assay, Real-time Polymerase Chain Reaction

30) Product Images from "Down Regulation of Wnt Signaling Mitigates Hypoxia-Induced Chemoresistance in Human Osteosarcoma Cells"

Article Title: Down Regulation of Wnt Signaling Mitigates Hypoxia-Induced Chemoresistance in Human Osteosarcoma Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0111431

Hypoxia results in chemoresistance of human OS cells to doxorubicin. A, Dose-response curves for the 143B and MNNG/HOS (mHOS) cell lines treated with increasing concentrations of doxorubicin under normoxic and hypoxic conditions (72 hour, 0.5% O 2 ). Luminescence (viability) was determined as a percent of untreated control (0 µM doxorubicin). B, Average half maximal inhibitory concentration (IC 50 ) values were obtained from the dose-response curves and compared between normoxic and hypoxic conditions for the cell lines MNNG/HOS (mHOS), 143B, and a patient-derived OS cell line, 206-2. Asterisks indicate statistical significance (**p
Figure Legend Snippet: Hypoxia results in chemoresistance of human OS cells to doxorubicin. A, Dose-response curves for the 143B and MNNG/HOS (mHOS) cell lines treated with increasing concentrations of doxorubicin under normoxic and hypoxic conditions (72 hour, 0.5% O 2 ). Luminescence (viability) was determined as a percent of untreated control (0 µM doxorubicin). B, Average half maximal inhibitory concentration (IC 50 ) values were obtained from the dose-response curves and compared between normoxic and hypoxic conditions for the cell lines MNNG/HOS (mHOS), 143B, and a patient-derived OS cell line, 206-2. Asterisks indicate statistical significance (**p

Techniques Used: Concentration Assay, Derivative Assay

Further Wnt/β-catenin signaling inhibition sensitizes hypoxic OS cells to doxorubicin. MG-63 OS cells were treated with increasing concentrations of doxorubicin under hypoxic conditions in the presence of the tankyrase inhibitor XAV939, the porcupine inhibitor IWP-2, or DMSO alone. Half maximal inhibitory concentrations (IC 50 ) were calculated, and the percent IC 50 relative to DMSO alone was determined. Asterisks indicate statistical significance (*p
Figure Legend Snippet: Further Wnt/β-catenin signaling inhibition sensitizes hypoxic OS cells to doxorubicin. MG-63 OS cells were treated with increasing concentrations of doxorubicin under hypoxic conditions in the presence of the tankyrase inhibitor XAV939, the porcupine inhibitor IWP-2, or DMSO alone. Half maximal inhibitory concentrations (IC 50 ) were calculated, and the percent IC 50 relative to DMSO alone was determined. Asterisks indicate statistical significance (*p

Techniques Used: Inhibition

31) Product Images from "Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to doxorubicin via Src-Stat3 inactivation in osteosarcoma"

Article Title: Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to doxorubicin via Src-Stat3 inactivation in osteosarcoma

Journal: Scientific Reports

doi: 10.1038/srep40187

AMBN suppresses colony formation and cell migration through the Src-Stat3 pathway in osteosarcoma cells. (A) Colony formation was assessed by soft-agar colony formation assay and representative colonies are shown (upper panels). Quantification of colony number and size is shown (lower graphs) ( N = 20). (B) Cell migration activity was examined by wound healing assay. Representative images at 5 h are shown (left panels) and wound areas were quantified (right graph) ( N = 3). Original magnification of the left panels: ×100. (C) Empty vector and Src-Y527F plasmid were transfected into AMBN-stable 143B-Luc cells, colony formation was assessed and representative colonies are shown (upper panels). Quantification of colony number and size is shown (lower graphs) ( N = 20). (D) Cell migration activity was examined. Representative images at 5 h are shown (left panels) and wound areas were quantified (right graph) ( N = 3). Original magnification of the left panels: ×100. (E) 143B-Luc cells were pretreated with SU6656 at indicated concentration for 24 h. The pretreated 143B-Luc cells were subsequently treated with DMSO or doxorubicin (0.5 μg/mL) for 24 h and the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3, and cleaved caspase-3 was examined. (F) Cell migration activity of pretreated 143B-Luc cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3). (G) Colony formation in pretreated 143B-Luc cells was analyzed and representative colonies were shown (upper panels). Quantification of colony number and size was shown (lower panels) ( N = 20). (H) 143B-Luc cells were pretreated with S3I-201 at indicated concentration for 24 h. The pretreated 143B-Luc cells were subsequently treated with doxorubicin (0.5 μg/mL) for 24 h and the expression of pY705-Stat3, total-Stat3 and cleaved caspase-3 was examined. (I) Cell migration activity of pretreated 143B-Luc cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3) . (J) Colony formation in pretreated 143B-Luc cells was analyzed and representative colonies were shown (upper panels). Quantification of colony number and size was shown (lower panels) ( N = 20). Mean ± SEM ( A–D,F,G,I , J ); ** P
Figure Legend Snippet: AMBN suppresses colony formation and cell migration through the Src-Stat3 pathway in osteosarcoma cells. (A) Colony formation was assessed by soft-agar colony formation assay and representative colonies are shown (upper panels). Quantification of colony number and size is shown (lower graphs) ( N = 20). (B) Cell migration activity was examined by wound healing assay. Representative images at 5 h are shown (left panels) and wound areas were quantified (right graph) ( N = 3). Original magnification of the left panels: ×100. (C) Empty vector and Src-Y527F plasmid were transfected into AMBN-stable 143B-Luc cells, colony formation was assessed and representative colonies are shown (upper panels). Quantification of colony number and size is shown (lower graphs) ( N = 20). (D) Cell migration activity was examined. Representative images at 5 h are shown (left panels) and wound areas were quantified (right graph) ( N = 3). Original magnification of the left panels: ×100. (E) 143B-Luc cells were pretreated with SU6656 at indicated concentration for 24 h. The pretreated 143B-Luc cells were subsequently treated with DMSO or doxorubicin (0.5 μg/mL) for 24 h and the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3, and cleaved caspase-3 was examined. (F) Cell migration activity of pretreated 143B-Luc cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3). (G) Colony formation in pretreated 143B-Luc cells was analyzed and representative colonies were shown (upper panels). Quantification of colony number and size was shown (lower panels) ( N = 20). (H) 143B-Luc cells were pretreated with S3I-201 at indicated concentration for 24 h. The pretreated 143B-Luc cells were subsequently treated with doxorubicin (0.5 μg/mL) for 24 h and the expression of pY705-Stat3, total-Stat3 and cleaved caspase-3 was examined. (I) Cell migration activity of pretreated 143B-Luc cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3) . (J) Colony formation in pretreated 143B-Luc cells was analyzed and representative colonies were shown (upper panels). Quantification of colony number and size was shown (lower panels) ( N = 20). Mean ± SEM ( A–D,F,G,I , J ); ** P

Techniques Used: Migration, Soft Agar Assay, Activity Assay, Wound Healing Assay, Plasmid Preparation, Transfection, Concentration Assay, Expressing

AMBN induces apoptosis and sensitivity to doxorubicin through the Src-Stat3 pathway in osteosarcoma cells. (A) The expression of AMBN at the protein level and AMBN, RUNX2, ALP, and OCN at the mRNA level among human osteosarcoma cell lines is shown. (B) The expression of AMBN, RUNX2, ALP, and OCN at the mRNA level in control and AMBN-stable 143B-Luc cells was examined. (C) Cell growth was counted on days 0, 1, 3, and 5 ( N = 3). (D) Cell cycle distributions were analyzed by PI staining and FACS, and quantified ( N = 3). (E) The apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, (F) and quantified ( N = 3). (G) Control and AMBN-stable 143B-Luc cells were treated with doxorubicin at indicated concentration for 48 hours, then the cells attached on the dishes were counted and quantified ( N = 3). (H) After the treatment with DMSO and doxorubicin (0.5 μg/mL) for 12 h, the apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, (I) and quantified ( N = 3). (J) The expression of pY416-Src and total-Src in control and AMBN-stable 143B-Luc cells after attachment on the culture dish (0, 30, 60 minutes) was examined. Relative expression of pY416-Src (Src activation) is shown. (K) Empty vector and Src-Y527F plasmid were transfected into control and AMBN-stable 143B-Luc cells, the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3 was examined. Relative expression of pY705-Stat3 (Stat3 activation) is shown. (L) Empty vector and Src-Y527F plasmid were transfected into AMBN-stable 143B-Luc cells, and the expression of pY416-Src, total-Src, and cleaved caspase-3 was evaluated (upper panel). The apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, and the representative results are summarized (lower graph) ( N = 3). (M) After the transfection of empty and Src-Y527F into control and AMBN-stable 143B-Luc cells, these cells were treated with DMSO and doxorubicin (0.5 μg/mL) for 24 h. The expression of cleaved caspase-3 was examined. Mean ± SEM ( C,D , F , G , I , L ); *** P
Figure Legend Snippet: AMBN induces apoptosis and sensitivity to doxorubicin through the Src-Stat3 pathway in osteosarcoma cells. (A) The expression of AMBN at the protein level and AMBN, RUNX2, ALP, and OCN at the mRNA level among human osteosarcoma cell lines is shown. (B) The expression of AMBN, RUNX2, ALP, and OCN at the mRNA level in control and AMBN-stable 143B-Luc cells was examined. (C) Cell growth was counted on days 0, 1, 3, and 5 ( N = 3). (D) Cell cycle distributions were analyzed by PI staining and FACS, and quantified ( N = 3). (E) The apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, (F) and quantified ( N = 3). (G) Control and AMBN-stable 143B-Luc cells were treated with doxorubicin at indicated concentration for 48 hours, then the cells attached on the dishes were counted and quantified ( N = 3). (H) After the treatment with DMSO and doxorubicin (0.5 μg/mL) for 12 h, the apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, (I) and quantified ( N = 3). (J) The expression of pY416-Src and total-Src in control and AMBN-stable 143B-Luc cells after attachment on the culture dish (0, 30, 60 minutes) was examined. Relative expression of pY416-Src (Src activation) is shown. (K) Empty vector and Src-Y527F plasmid were transfected into control and AMBN-stable 143B-Luc cells, the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3 was examined. Relative expression of pY705-Stat3 (Stat3 activation) is shown. (L) Empty vector and Src-Y527F plasmid were transfected into AMBN-stable 143B-Luc cells, and the expression of pY416-Src, total-Src, and cleaved caspase-3 was evaluated (upper panel). The apoptotic cell ratio was analyzed by annexin-V/7-AAD staining and FACS, and the representative results are summarized (lower graph) ( N = 3). (M) After the transfection of empty and Src-Y527F into control and AMBN-stable 143B-Luc cells, these cells were treated with DMSO and doxorubicin (0.5 μg/mL) for 24 h. The expression of cleaved caspase-3 was examined. Mean ± SEM ( C,D , F , G , I , L ); *** P

Techniques Used: Expressing, ALP Assay, Staining, FACS, Concentration Assay, Activation Assay, Plasmid Preparation, Transfection

AMBN knockdown suppresses apoptosis, sensitivity to doxorubicin, and promotes cell migration and colony formation through the Src-Stat3 pathway in NOS-1 cells. ( A ) The expression of AMBN, RUNX2, ALP, and OCN at the mRNA level (left panel) and AMBN, pY705-Stat3, total-Stat3, pY416-Src, total-Src and cleaved caspase-3 at the protein level in shscramble, shAMBN1, and shAMBN2 NOS-1 cells was examined (right panel). ( B , F ) shAMBN2 NOS-1 cells were pretreated with SU6656 or S3I-201 at indicated concentration for 24 h. The pretreated shAMBN-2 NOS-1 cells were subsequently treated with DMSO or doxorubicin (0.5 μg/mL) for 24 h and the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3, and cleaved caspase-3 was examined. ( C , G ) shscramble and shAMBN-2 NOS-1 cells were treated with SU6656 o S3I-201 at indicated concentration and cell growth was counted on days 0, 1, 2, and 3 ( N = 3). ( D , H ) Cell migration activity of pretreated shscramble and shAMBN-2 NOS-1 cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3). ( E , I ) Colony formation in pretreated shscramble and shAMBN-2 NOS-1 cells was analyzed. Quantification of colony number (left panel) and size (right panel) was shown ( N = 20). Mean ± SEM ( C–E , G–I ); ** P
Figure Legend Snippet: AMBN knockdown suppresses apoptosis, sensitivity to doxorubicin, and promotes cell migration and colony formation through the Src-Stat3 pathway in NOS-1 cells. ( A ) The expression of AMBN, RUNX2, ALP, and OCN at the mRNA level (left panel) and AMBN, pY705-Stat3, total-Stat3, pY416-Src, total-Src and cleaved caspase-3 at the protein level in shscramble, shAMBN1, and shAMBN2 NOS-1 cells was examined (right panel). ( B , F ) shAMBN2 NOS-1 cells were pretreated with SU6656 or S3I-201 at indicated concentration for 24 h. The pretreated shAMBN-2 NOS-1 cells were subsequently treated with DMSO or doxorubicin (0.5 μg/mL) for 24 h and the expression of pY416-Src, total-Src, pY705-Stat3, total-Stat3, and cleaved caspase-3 was examined. ( C , G ) shscramble and shAMBN-2 NOS-1 cells were treated with SU6656 o S3I-201 at indicated concentration and cell growth was counted on days 0, 1, 2, and 3 ( N = 3). ( D , H ) Cell migration activity of pretreated shscramble and shAMBN-2 NOS-1 cells was examined. Wound areas at 5 h were quantified in the graphs ( N = 3). ( E , I ) Colony formation in pretreated shscramble and shAMBN-2 NOS-1 cells was analyzed. Quantification of colony number (left panel) and size (right panel) was shown ( N = 20). Mean ± SEM ( C–E , G–I ); ** P

Techniques Used: Migration, Expressing, ALP Assay, Concentration Assay, Activity Assay

32) Product Images from "Systematic discovery of drug action mechanisms by an integrated chemical genomics approach: identification of functional disparities between azacytidine and decitabine"

Article Title: Systematic discovery of drug action mechanisms by an integrated chemical genomics approach: identification of functional disparities between azacytidine and decitabine

Journal: Oncotarget

doi: 10.18632/oncotarget.8455

The relationship between apoptosis and autophagy induced by azacytidine (AZA) ( A ) HCT116 cells were treated with different doses of doxorubicin for 72 h, and the cell viability was analyzed by an MTT assay. ( B ) HCT116 cells were treated with different doses of AZA or decitabine (DAC), or 0.5 μM doxorubicin for 24 and 48 h, and whole-cell lysates were subjected to a Western blot analysis using antibodies against PARP1, LC3B, or GAPDH. ( C ) HCT116 cells were pretreated with 5 mM 3-MA or 50 μM Z-DEVD-FMK for 1 h and then exposed to 50 μM AZA for 24 h. Whole-cell lysates were subjected to a Western blot analysis using antibodies against PARP1, LC3B, or GAPDH. ( D ) ATG7-WT and ATG7-KO DLD-1 cells were treated with different doses of AZA for 72 h, and cell viability was analyzed by an MTT assay.
Figure Legend Snippet: The relationship between apoptosis and autophagy induced by azacytidine (AZA) ( A ) HCT116 cells were treated with different doses of doxorubicin for 72 h, and the cell viability was analyzed by an MTT assay. ( B ) HCT116 cells were treated with different doses of AZA or decitabine (DAC), or 0.5 μM doxorubicin for 24 and 48 h, and whole-cell lysates were subjected to a Western blot analysis using antibodies against PARP1, LC3B, or GAPDH. ( C ) HCT116 cells were pretreated with 5 mM 3-MA or 50 μM Z-DEVD-FMK for 1 h and then exposed to 50 μM AZA for 24 h. Whole-cell lysates were subjected to a Western blot analysis using antibodies against PARP1, LC3B, or GAPDH. ( D ) ATG7-WT and ATG7-KO DLD-1 cells were treated with different doses of AZA for 72 h, and cell viability was analyzed by an MTT assay.

Techniques Used: MTT Assay, Western Blot

Effects of azacytidine (AZA) and decitabine (DAC) on caspase-3/7 activity HCT116 cells were treated with different doses of AZA or DAC, or 0.5 μM doxorubicin for 24 and 48 h, and the caspase-3/7 activity was analyzed by flow cytometry as described in “Materials and Methods”.
Figure Legend Snippet: Effects of azacytidine (AZA) and decitabine (DAC) on caspase-3/7 activity HCT116 cells were treated with different doses of AZA or DAC, or 0.5 μM doxorubicin for 24 and 48 h, and the caspase-3/7 activity was analyzed by flow cytometry as described in “Materials and Methods”.

Techniques Used: Activity Assay, Flow Cytometry, Cytometry

33) Product Images from "Targeting ABCB1-mediated tumor multidrug resistance by CRISPR/Cas9-based genome editing"

Article Title: Targeting ABCB1-mediated tumor multidrug resistance by CRISPR/Cas9-based genome editing

Journal: American Journal of Translational Research

doi:

Knockout of ABCB1 by CRISPR/Cas9 system enhances the sensitivity of ABCB1 substrate chemotherapeutic agents in MDR cancer cells. Cells were treated with the indicated concentrations of vincristine, doxorubicin or cisplatin for 72 hours, and cell survival
Figure Legend Snippet: Knockout of ABCB1 by CRISPR/Cas9 system enhances the sensitivity of ABCB1 substrate chemotherapeutic agents in MDR cancer cells. Cells were treated with the indicated concentrations of vincristine, doxorubicin or cisplatin for 72 hours, and cell survival

Techniques Used: Knock-Out, CRISPR

Knockout of ABCB1 by CRISPR/Cas9 system increases the intracellular accumulation of rhodamine 123 and doxorubicin in MDR cancer cells. Cells were incubated with 10 μM rhodamine 123 or doxorubicin for 2 hours at 37°C, measured by FCM and
Figure Legend Snippet: Knockout of ABCB1 by CRISPR/Cas9 system increases the intracellular accumulation of rhodamine 123 and doxorubicin in MDR cancer cells. Cells were incubated with 10 μM rhodamine 123 or doxorubicin for 2 hours at 37°C, measured by FCM and

Techniques Used: Knock-Out, CRISPR, Incubation

34) Product Images from "A Biomaterial Screening Approach Reveals Microenvironmental Mechanisms of Drug Resistance"

Article Title: A Biomaterial Screening Approach Reveals Microenvironmental Mechanisms of Drug Resistance

Journal: Integrative biology : quantitative biosciences from nano to macro

doi: 10.1039/c7ib00128b

Drug response is dependent upon the biomaterial screening platform a. Schematic of biomaterial drug screening platforms, including TCPS, 2D hydrogels linked with collagen I, and 3D hydrogels with RGD for cell adhesion, either with encapsulated single cells or tumor spheroids. Each hydrogel condition was screened at two different moduli (2D: 10 or 33 kPa, 3D: 3 or 5 kPa). b. Quantification of mean spheroid diameter for MDA-MB-231 spheroid growth in polyNIPAAM gels over 14 days. c. Viability of MDA-MB-231 spheroid after 14 days of growth in polyNIPAAM, and encapsulation in 3 kPa 3D PEG-MAL hydrogel for 3 days. Green: live cells, red: dead cells. Scale: 100 µm. d. Experimental time investment required for the different screening platforms. Timeline displays preparation time required for each system prior to treating with varying concentrations of drug. e–f. SkBr3 (e) and MDA-MB-231 (f) proliferation after 3 days of culture (top row), and GR 50 in response to doxorubicin, temsirolimus, sorafenib, and lapatinib across the different biomaterial platforms. Red: increase from TCPS control (resistance compared to TCPS), blue: decrease from TCPS control (sensitivity compared to TCPS). TC: TCPS, 10: 10 kPa 2D hydrogel, 33: 33 kPa 2D hydrogel, 3: 3 kPa 3D hydrogel, 5: 5 kPa 3D hydrogel, +FBS: cells were treated in 10% serum-containing medium. Unless noted by +FBS, all cells were treated with drugs in serum-free medium containing EGF and PDGF-BB.
Figure Legend Snippet: Drug response is dependent upon the biomaterial screening platform a. Schematic of biomaterial drug screening platforms, including TCPS, 2D hydrogels linked with collagen I, and 3D hydrogels with RGD for cell adhesion, either with encapsulated single cells or tumor spheroids. Each hydrogel condition was screened at two different moduli (2D: 10 or 33 kPa, 3D: 3 or 5 kPa). b. Quantification of mean spheroid diameter for MDA-MB-231 spheroid growth in polyNIPAAM gels over 14 days. c. Viability of MDA-MB-231 spheroid after 14 days of growth in polyNIPAAM, and encapsulation in 3 kPa 3D PEG-MAL hydrogel for 3 days. Green: live cells, red: dead cells. Scale: 100 µm. d. Experimental time investment required for the different screening platforms. Timeline displays preparation time required for each system prior to treating with varying concentrations of drug. e–f. SkBr3 (e) and MDA-MB-231 (f) proliferation after 3 days of culture (top row), and GR 50 in response to doxorubicin, temsirolimus, sorafenib, and lapatinib across the different biomaterial platforms. Red: increase from TCPS control (resistance compared to TCPS), blue: decrease from TCPS control (sensitivity compared to TCPS). TC: TCPS, 10: 10 kPa 2D hydrogel, 33: 33 kPa 2D hydrogel, 3: 3 kPa 3D hydrogel, 5: 5 kPa 3D hydrogel, +FBS: cells were treated in 10% serum-containing medium. Unless noted by +FBS, all cells were treated with drugs in serum-free medium containing EGF and PDGF-BB.

Techniques Used: Multiple Displacement Amplification

35) Product Images from "Layer-by-Layer Nanoparticles for Systemic Codelivery of an Anticancer Drug and siRNA for Potential Triple-Negative Breast Cancer Treatment"

Article Title: Layer-by-Layer Nanoparticles for Systemic Codelivery of an Anticancer Drug and siRNA for Potential Triple-Negative Breast Cancer Treatment

Journal: ACS nano

doi: 10.1021/nn4047925

Codelivery of siRNA and doxorubicin using LbL liposomes as potential TNBC therapeutics
Figure Legend Snippet: Codelivery of siRNA and doxorubicin using LbL liposomes as potential TNBC therapeutics

Techniques Used:

Assessment of codelivery of MRP1 siRNA and doxorubicin using Dox-liposome/PLA/siRNA/PLA/HA LbL liposomes for combination therapy to TNBC in mice models. (A, B) Change in tumor volume in nude mice bearing subcutaneous MDA-MB-468 xenografts treated with
Figure Legend Snippet: Assessment of codelivery of MRP1 siRNA and doxorubicin using Dox-liposome/PLA/siRNA/PLA/HA LbL liposomes for combination therapy to TNBC in mice models. (A, B) Change in tumor volume in nude mice bearing subcutaneous MDA-MB-468 xenografts treated with

Techniques Used: Proximity Ligation Assay, Mouse Assay, Multiple Displacement Amplification

The co-delivery of siRNA and doxorubicin using the modular Dox-liposome/PLA/siRNA/PLA/HA LbL nanoparticle platform. (A) Design schematics of the siRNA-doxorubicin LbL liposomes. (B) Release profile of the two therapeutics components: siRNA and doxorubicin
Figure Legend Snippet: The co-delivery of siRNA and doxorubicin using the modular Dox-liposome/PLA/siRNA/PLA/HA LbL nanoparticle platform. (A) Design schematics of the siRNA-doxorubicin LbL liposomes. (B) Release profile of the two therapeutics components: siRNA and doxorubicin

Techniques Used: Proximity Ligation Assay

36) Product Images from "Chemotherapy-Induced Tunneling Nanotubes Mediate Intercellular Drug Efflux in Pancreatic Cancer"

Article Title: Chemotherapy-Induced Tunneling Nanotubes Mediate Intercellular Drug Efflux in Pancreatic Cancer

Journal: Scientific Reports

doi: 10.1038/s41598-018-27649-x

Variable dose-dependent response of TNTs forming after exposure to the chemotherapeutic drug doxorubicin. ( A ) Representative images of TNTs transmitting autofluorescing (red) doxorubicin between S2013 cells. Images were taken using a Zeiss Axio widefield microscope. Scale bars = 50 μm. ( B , C ) Scatter-plot graph depicting the median number of TNTs/cell (TNT index) over time, comparing results for the S2013 (Panel B) and MIA PaCa-2 (Panel C) cell lines after exposure to six concentrations of doxorubicin. This experiment was done in triplicate, with a sample size of 18 fields of view per dose/per time point.
Figure Legend Snippet: Variable dose-dependent response of TNTs forming after exposure to the chemotherapeutic drug doxorubicin. ( A ) Representative images of TNTs transmitting autofluorescing (red) doxorubicin between S2013 cells. Images were taken using a Zeiss Axio widefield microscope. Scale bars = 50 μm. ( B , C ) Scatter-plot graph depicting the median number of TNTs/cell (TNT index) over time, comparing results for the S2013 (Panel B) and MIA PaCa-2 (Panel C) cell lines after exposure to six concentrations of doxorubicin. This experiment was done in triplicate, with a sample size of 18 fields of view per dose/per time point.

Techniques Used: Microscopy

TNTs act as a direct conduit for intercellular transfer and redistribution of the chemotherapeutic drug doxorubicin. ( A ) TNT formation and intercellular transfer of doxorubicin between S2013 pancreatic adenocarcinoma cells. ( B ) Composite of serial images from time-lapse microscopy demonstrating intercellular transfer of doxorubicin from a chemoresistant ovarian cancer cell (SKOV3) to a chemosensitive cell (A2780) via a TNT, resulting in cell death of the chemosensitive cell. Images were taken every 15 minutes for 24 hours using a wide-field Zeiss Axio200M microscope.
Figure Legend Snippet: TNTs act as a direct conduit for intercellular transfer and redistribution of the chemotherapeutic drug doxorubicin. ( A ) TNT formation and intercellular transfer of doxorubicin between S2013 pancreatic adenocarcinoma cells. ( B ) Composite of serial images from time-lapse microscopy demonstrating intercellular transfer of doxorubicin from a chemoresistant ovarian cancer cell (SKOV3) to a chemosensitive cell (A2780) via a TNT, resulting in cell death of the chemosensitive cell. Images were taken every 15 minutes for 24 hours using a wide-field Zeiss Axio200M microscope.

Techniques Used: Activated Clotting Time Assay, Time-lapse Microscopy, Microscopy

37) Product Images from "Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis"

Article Title: Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis

Journal: EMBO Molecular Medicine

doi: 10.15252/emmm.201809003

Expression of stem cell signature and JNK signaling in breast cancer cells treated with chemotherapy GSEA graph showing enrichment of a mammary stem cell signature (mammary repopulating units, MRU) (Stingl et al , 2006 ), in MDA231‐LM2 cells treated with paclitaxel (PAX). NES, normalized enrichment score. P ‐value was determined by random permutation test. GSEA of JNK signature in the gene expression data set of paclitaxel‐treated MDA231‐LM2 cells. NES, normalized enrichment score. P ‐value was determined by random permutation test. Western blot analysis of p‐JNK, JNK, p‐c‐Jun, and c‐Jun in SUM159‐LM1 cells treated with incremental concentrations of doxorubicin (DOXO). Tubulin was used as a loading control. Source data are available online for this figure.
Figure Legend Snippet: Expression of stem cell signature and JNK signaling in breast cancer cells treated with chemotherapy GSEA graph showing enrichment of a mammary stem cell signature (mammary repopulating units, MRU) (Stingl et al , 2006 ), in MDA231‐LM2 cells treated with paclitaxel (PAX). NES, normalized enrichment score. P ‐value was determined by random permutation test. GSEA of JNK signature in the gene expression data set of paclitaxel‐treated MDA231‐LM2 cells. NES, normalized enrichment score. P ‐value was determined by random permutation test. Western blot analysis of p‐JNK, JNK, p‐c‐Jun, and c‐Jun in SUM159‐LM1 cells treated with incremental concentrations of doxorubicin (DOXO). Tubulin was used as a loading control. Source data are available online for this figure.

Techniques Used: Expressing, Western Blot

38) Product Images from "Anthocyanin Attenuates Doxorubicin-Induced Cardiomyotoxicity via Estrogen Receptor-α/β and Stabilizes HSF1 to Inhibit the IGF-IIR Apoptotic Pathway"

Article Title: Anthocyanin Attenuates Doxorubicin-Induced Cardiomyotoxicity via Estrogen Receptor-α/β and Stabilizes HSF1 to Inhibit the IGF-IIR Apoptotic Pathway

Journal: International Journal of Molecular Sciences

doi: 10.3390/ijms17091588

Schematic diagram of how ACN attenuates doxorubicin-induced cardiomyotoxicity through ERα/β to up-regulate CHIP-mediated HSF1 nuclear translocation and SIRT1-mediated HSF1 activation to inhibit the IGF-IIR apoptotic pathway.
Figure Legend Snippet: Schematic diagram of how ACN attenuates doxorubicin-induced cardiomyotoxicity through ERα/β to up-regulate CHIP-mediated HSF1 nuclear translocation and SIRT1-mediated HSF1 activation to inhibit the IGF-IIR apoptotic pathway.

Techniques Used: Chromatin Immunoprecipitation, Translocation Assay, Activation Assay

Dox stimulated the insulin-like growth factor II receptor (IGF-IIR) apoptotic pathway and repressed the expression of the estrogen receptors (ERs). ( A ) H9c2 cells are treated with different concentrations of doxorubicin for 24 h; the protein level of CHIP, HSF1, IGF-IIR, active caspase 3, and p-Akt is measured by immunoblotting. Quantification of these results is shown right ( n = 3). * p
Figure Legend Snippet: Dox stimulated the insulin-like growth factor II receptor (IGF-IIR) apoptotic pathway and repressed the expression of the estrogen receptors (ERs). ( A ) H9c2 cells are treated with different concentrations of doxorubicin for 24 h; the protein level of CHIP, HSF1, IGF-IIR, active caspase 3, and p-Akt is measured by immunoblotting. Quantification of these results is shown right ( n = 3). * p

Techniques Used: Expressing, Chromatin Immunoprecipitation

The effects of anthocyanin treatment were attenuated by the estrogen receptor antagonist ICI 182,780. ( A ) H9c2 cells were pre-treated with 1 µM ICI 182,780 for 1 h, followed by treatment with doxorubicin at 1 µM and incubation for 6 h. Then, the medium was changed to fresh medium, anthocyanin at 40 µg/mL was added, and the cells were incubated for 18 h before measurement by immunoblotting. Quantification of these results is shown right ( n = 3). * p
Figure Legend Snippet: The effects of anthocyanin treatment were attenuated by the estrogen receptor antagonist ICI 182,780. ( A ) H9c2 cells were pre-treated with 1 µM ICI 182,780 for 1 h, followed by treatment with doxorubicin at 1 µM and incubation for 6 h. Then, the medium was changed to fresh medium, anthocyanin at 40 µg/mL was added, and the cells were incubated for 18 h before measurement by immunoblotting. Quantification of these results is shown right ( n = 3). * p

Techniques Used: Incubation

Protein expression of the left ventricles of rat hearts after six weeks of doxorubicin and anthocyanin treatment. ( A , B ) The left ventricles of hearts were excised and homogenized. The cell lysates were quantified and analyzed via immunoblotting. The expression of the IGF-IIR signaling pathway protein and the expression of the apoptosis marker caspase-3 and ERs were estimated via immunoblotting. Quantification of the results is shown right ( n = 3 per group). * p
Figure Legend Snippet: Protein expression of the left ventricles of rat hearts after six weeks of doxorubicin and anthocyanin treatment. ( A , B ) The left ventricles of hearts were excised and homogenized. The cell lysates were quantified and analyzed via immunoblotting. The expression of the IGF-IIR signaling pathway protein and the expression of the apoptosis marker caspase-3 and ERs were estimated via immunoblotting. Quantification of the results is shown right ( n = 3 per group). * p

Techniques Used: Expressing, Marker

Anthocyanin enhanced ER expression and attenuated the IGF-IIR apoptotic pathway. ( A ) After H9c2 cells are treated with 1 µM doxorubicin for 6 and 12 h, they are washed with PBS, and then, fresh medium is added, followed by post-treatment with anthocyanin 20 and 40 µg/mL and incubation of cells for 24 h after doxorubicin treatment. The ERα and ERβ protein levels were measured. Quantification of these results is shown right ( n = 3). * p
Figure Legend Snippet: Anthocyanin enhanced ER expression and attenuated the IGF-IIR apoptotic pathway. ( A ) After H9c2 cells are treated with 1 µM doxorubicin for 6 and 12 h, they are washed with PBS, and then, fresh medium is added, followed by post-treatment with anthocyanin 20 and 40 µg/mL and incubation of cells for 24 h after doxorubicin treatment. The ERα and ERβ protein levels were measured. Quantification of these results is shown right ( n = 3). * p

Techniques Used: Expressing, Incubation

Echocardiographic assessments and histopathological analysis of rat left ventricular cells after doxorubicin and anthocyanin treatment. ( A ) The schematic procedure of DOX and HSF1A administration; ( B ) histopathologic analysis of heart tissue sections stained with H and E. Magnification: 200×; bars = 50 µm. An enlarged interstitium was observed in the doxorubicin-treated rat hearts, and the arrows indicate the myocardial interstitium. The expression of TUNEL + cardiomyocytes and SIRT1 expression were evaluated by immunohistochemistry (IHC) and TUNEL assay. Quantification of TUNEL + cardiomyocytes from each group is shown right ( n = 3 per group). These data were obtained from at least three independent experiments and values represent the means ± S.D. ** p
Figure Legend Snippet: Echocardiographic assessments and histopathological analysis of rat left ventricular cells after doxorubicin and anthocyanin treatment. ( A ) The schematic procedure of DOX and HSF1A administration; ( B ) histopathologic analysis of heart tissue sections stained with H and E. Magnification: 200×; bars = 50 µm. An enlarged interstitium was observed in the doxorubicin-treated rat hearts, and the arrows indicate the myocardial interstitium. The expression of TUNEL + cardiomyocytes and SIRT1 expression were evaluated by immunohistochemistry (IHC) and TUNEL assay. Quantification of TUNEL + cardiomyocytes from each group is shown right ( n = 3 per group). These data were obtained from at least three independent experiments and values represent the means ± S.D. ** p

Techniques Used: Staining, Expressing, TUNEL Assay, Immunohistochemistry

39) Product Images from "Trojan Horse nanotheranostics with dual transformability and multifunctionality for highly effective cancer treatment"

Article Title: Trojan Horse nanotheranostics with dual transformability and multifunctionality for highly effective cancer treatment

Journal: Nature Communications

doi: 10.1038/s41467-018-06093-5

Schematic illustration of the Trojan-Horse nanoparticles. Image illustration of the functionalities of the building blocks and construction of the Trojan-Horse nanoparticles (pPhD NPs), and their capabilities to overcome a series of biological barriers through TME responsiveness, de-PEGylation/cross-linkage, transformability, superior penetrations, enhanced cell internalisation, intracellular drug release for multimodal imaging and trimodality therapies. Abbreviations: PDT photodynamic therapy, PTT photothermal therapy, NIRFI near-infrared fluorescence imaging, MRI magnetic resonance imaging, TME tumour microenvironment, Red square denotes Phy, and blue circle denotes DOX, PhD pheophorbide a-hydrazone-doxorubicin, upPhD NPs unPEGylated PhD NPs, pPhD NPs PEGylated PhD NPs, 1 O 2 reactive oxygen species
Figure Legend Snippet: Schematic illustration of the Trojan-Horse nanoparticles. Image illustration of the functionalities of the building blocks and construction of the Trojan-Horse nanoparticles (pPhD NPs), and their capabilities to overcome a series of biological barriers through TME responsiveness, de-PEGylation/cross-linkage, transformability, superior penetrations, enhanced cell internalisation, intracellular drug release for multimodal imaging and trimodality therapies. Abbreviations: PDT photodynamic therapy, PTT photothermal therapy, NIRFI near-infrared fluorescence imaging, MRI magnetic resonance imaging, TME tumour microenvironment, Red square denotes Phy, and blue circle denotes DOX, PhD pheophorbide a-hydrazone-doxorubicin, upPhD NPs unPEGylated PhD NPs, pPhD NPs PEGylated PhD NPs, 1 O 2 reactive oxygen species

Techniques Used: Imaging, Fluorescence, Magnetic Resonance Imaging

40) Product Images from "Aberrant expression and biological significance of Sox2, an embryonic stem cell transcriptional factor, in ALK-positive anaplastic large cell lymphoma"

Article Title: Aberrant expression and biological significance of Sox2, an embryonic stem cell transcriptional factor, in ALK-positive anaplastic large cell lymphoma

Journal: Blood Cancer Journal

doi: 10.1038/bcj.2012.27

Sox2 transcriptional activity correlates with the sensitivity to doxorubicin. Sox2 active subset of cells in both Karpas 299 ( a ) and SUP-M2 ( b ) were more resistant to doxorubicin as compared with the Sox2 inactive subset. Results shown are representative of three independent experiments.
Figure Legend Snippet: Sox2 transcriptional activity correlates with the sensitivity to doxorubicin. Sox2 active subset of cells in both Karpas 299 ( a ) and SUP-M2 ( b ) were more resistant to doxorubicin as compared with the Sox2 inactive subset. Results shown are representative of three independent experiments.

Techniques Used: Activity Assay

41) Product Images from "Radiofrequency-triggered drug release from nanoliposomes with millimeter-scale resolution using a superimposed static gating field"

Article Title: Radiofrequency-triggered drug release from nanoliposomes with millimeter-scale resolution using a superimposed static gating field

Journal: Small (Weinheim an der Bergstrasse, Germany)

doi: 10.1002/smll.201802563

Spatially targeted doxorubicin release from thermally sensitive liposomes. (a) The cell viability curve for doxorubicin-loaded liposomes exposed to the AMF within the targeting region of the device is shifted left compared to liposomes at the edge. The concentration of doxorubicin-loaded liposomes exposed to the device at the center and edge are matched. Therefore, the total doxorubicin concentration is similarly matched between the center and edge, and any difference between cell viability at each concentration is due to differences in AMF-induced doxorubicin release between the center and the edge of the device. There is no decrease in cell viability observed when using blank liposomes loaded with PBS, or when using PBS only, either at the center or the edge. (b) Doxorubicin-loaded liposomes exposed to the AMF at the edge of the device have an IC50 of 4.44 ± 0.87 μM, while the same liposomes exposed to the AMF at the center targeting region of the device have an IC50 of 1.75 ± 0.37 μM; p = 0.0078. This corresponds to a therapeutic index of > 2.5 in Huh7 hepatocellular carcinoma cells. n = 3.
Figure Legend Snippet: Spatially targeted doxorubicin release from thermally sensitive liposomes. (a) The cell viability curve for doxorubicin-loaded liposomes exposed to the AMF within the targeting region of the device is shifted left compared to liposomes at the edge. The concentration of doxorubicin-loaded liposomes exposed to the device at the center and edge are matched. Therefore, the total doxorubicin concentration is similarly matched between the center and edge, and any difference between cell viability at each concentration is due to differences in AMF-induced doxorubicin release between the center and the edge of the device. There is no decrease in cell viability observed when using blank liposomes loaded with PBS, or when using PBS only, either at the center or the edge. (b) Doxorubicin-loaded liposomes exposed to the AMF at the edge of the device have an IC50 of 4.44 ± 0.87 μM, while the same liposomes exposed to the AMF at the center targeting region of the device have an IC50 of 1.75 ± 0.37 μM; p = 0.0078. This corresponds to a therapeutic index of > 2.5 in Huh7 hepatocellular carcinoma cells. n = 3.

Techniques Used: Concentration Assay

42) Product Images from "Radiofrequency-triggered drug release from nanoliposomes with millimeter-scale resolution using a superimposed static gating field"

Article Title: Radiofrequency-triggered drug release from nanoliposomes with millimeter-scale resolution using a superimposed static gating field

Journal: Small (Weinheim an der Bergstrasse, Germany)

doi: 10.1002/smll.201802563

Spatially targeted doxorubicin release from thermally sensitive liposomes. (a) The cell viability curve for doxorubicin-loaded liposomes exposed to the AMF within the targeting region of the device is shifted left compared to liposomes at the edge. The concentration of doxorubicin-loaded liposomes exposed to the device at the center and edge are matched. Therefore, the total doxorubicin concentration is similarly matched between the center and edge, and any difference between cell viability at each concentration is due to differences in AMF-induced doxorubicin release between the center and the edge of the device. There is no decrease in cell viability observed when using blank liposomes loaded with PBS, or when using PBS only, either at the center or the edge. (b) Doxorubicin-loaded liposomes exposed to the AMF at the edge of the device have an IC50 of 4.44 ± 0.87 μM, while the same liposomes exposed to the AMF at the center targeting region of the device have an IC50 of 1.75 ± 0.37 μM; p = 0.0078. This corresponds to a therapeutic index of > 2.5 in Huh7 hepatocellular carcinoma cells. n = 3.
Figure Legend Snippet: Spatially targeted doxorubicin release from thermally sensitive liposomes. (a) The cell viability curve for doxorubicin-loaded liposomes exposed to the AMF within the targeting region of the device is shifted left compared to liposomes at the edge. The concentration of doxorubicin-loaded liposomes exposed to the device at the center and edge are matched. Therefore, the total doxorubicin concentration is similarly matched between the center and edge, and any difference between cell viability at each concentration is due to differences in AMF-induced doxorubicin release between the center and the edge of the device. There is no decrease in cell viability observed when using blank liposomes loaded with PBS, or when using PBS only, either at the center or the edge. (b) Doxorubicin-loaded liposomes exposed to the AMF at the edge of the device have an IC50 of 4.44 ± 0.87 μM, while the same liposomes exposed to the AMF at the center targeting region of the device have an IC50 of 1.75 ± 0.37 μM; p = 0.0078. This corresponds to a therapeutic index of > 2.5 in Huh7 hepatocellular carcinoma cells. n = 3.

Techniques Used: Concentration Assay

43) Product Images from "Temporally sequenced anticancer drugs overcome adaptive resistance by targeting a vulnerable chemotherapy-induced phenotypic transition"

Article Title: Temporally sequenced anticancer drugs overcome adaptive resistance by targeting a vulnerable chemotherapy-induced phenotypic transition

Journal: Nature Communications

doi: 10.1038/ncomms7139

Taxane chemotherapy induces phenotypic cell state transition and adaptive resistance. ( a ) Schematic of human explant model to evaluate response of refractory human tissue to anticancer agents. Tumour biopsies were cut into ~200 mM-thick sections and cultured in microwells coated with tumour matrix and media supplemented with autologous serum. ( b ) Representative immunohistochemistry (IHC) of primary human breast tumour explants shows induction of CD44 and CD24 cell surface expression following 72 h treatment with docetaxel versus vehicle. × 40 Scale bar, 50 μm inset show higher magnification, × 100 ( c , d ) Graph shows quantification of CD44 and CD24 levels in the primary tumour explant studies, ( N =14 patients). Black and red points denote the protein levels measured by IHC score in a tumour explant in vehicle- and docetaxel-treated groups. Each number denotes a patient. The orange arrows denote patients who were taxane-treatment naive, whereas those denoted with black arrows received a taxane. ( e ) Representative IHC from explant culture shows effect of different drug treatments (3.4 μM docetaxel, 5.6 μM doxorubicin) on the expression of CD44 and cleaved (cl) caspase 3 in corresponding serial sections. Gem, gemcitabine. × 40 magnification Scale bar, 50 μm. Inset shows higher magnification × 100 ( f ) Graph shows the quantification of CD44 and cleaved caspase 3 expression in the explants treated with docetaxel ( n =9) or a combination of gemcitabine+carboplatin ( n =2). Data shows mean±s.e.m. ( g ) Schematic shows generation of drug-tolerant cells (DTCs) selected acutely using high-concentration docetaxel chemotherapy in vitro. Cells were cultured in 100 μM (~20X IC 50 ) docetaxel. Cells surviving by day 4 were quiescent and considered as drug-tolerant cells (DTCs). Growing out the DTCs over 35 days resulted in restoring parental properties. ( h ) Graph shows MTS cell viability analysis of parental cells and DTCs generated from of MDA-MB-231 breast cancer cells following incubation (48 h) with different tubulin-binding chemotherapeutics at indicated concentration range. ( i ) Confocal images show expression levels of CD44 and CD24 in parental cells and DTCs generated from MDA-MB-468s. Scale bar, 18 μm ( j ) The population percentage of CD44 Hi CD24 Hi cells in parental and DTCs generated from an array of luminal and basal breast cancer cell lines. Data shown are mean±s.e.m., n =3 ( P
Figure Legend Snippet: Taxane chemotherapy induces phenotypic cell state transition and adaptive resistance. ( a ) Schematic of human explant model to evaluate response of refractory human tissue to anticancer agents. Tumour biopsies were cut into ~200 mM-thick sections and cultured in microwells coated with tumour matrix and media supplemented with autologous serum. ( b ) Representative immunohistochemistry (IHC) of primary human breast tumour explants shows induction of CD44 and CD24 cell surface expression following 72 h treatment with docetaxel versus vehicle. × 40 Scale bar, 50 μm inset show higher magnification, × 100 ( c , d ) Graph shows quantification of CD44 and CD24 levels in the primary tumour explant studies, ( N =14 patients). Black and red points denote the protein levels measured by IHC score in a tumour explant in vehicle- and docetaxel-treated groups. Each number denotes a patient. The orange arrows denote patients who were taxane-treatment naive, whereas those denoted with black arrows received a taxane. ( e ) Representative IHC from explant culture shows effect of different drug treatments (3.4 μM docetaxel, 5.6 μM doxorubicin) on the expression of CD44 and cleaved (cl) caspase 3 in corresponding serial sections. Gem, gemcitabine. × 40 magnification Scale bar, 50 μm. Inset shows higher magnification × 100 ( f ) Graph shows the quantification of CD44 and cleaved caspase 3 expression in the explants treated with docetaxel ( n =9) or a combination of gemcitabine+carboplatin ( n =2). Data shows mean±s.e.m. ( g ) Schematic shows generation of drug-tolerant cells (DTCs) selected acutely using high-concentration docetaxel chemotherapy in vitro. Cells were cultured in 100 μM (~20X IC 50 ) docetaxel. Cells surviving by day 4 were quiescent and considered as drug-tolerant cells (DTCs). Growing out the DTCs over 35 days resulted in restoring parental properties. ( h ) Graph shows MTS cell viability analysis of parental cells and DTCs generated from of MDA-MB-231 breast cancer cells following incubation (48 h) with different tubulin-binding chemotherapeutics at indicated concentration range. ( i ) Confocal images show expression levels of CD44 and CD24 in parental cells and DTCs generated from MDA-MB-468s. Scale bar, 18 μm ( j ) The population percentage of CD44 Hi CD24 Hi cells in parental and DTCs generated from an array of luminal and basal breast cancer cell lines. Data shown are mean±s.e.m., n =3 ( P

Techniques Used: Cell Culture, Immunohistochemistry, Expressing, Concentration Assay, In Vitro, Generated, Multiple Displacement Amplification, Incubation, Binding Assay

44) Product Images from "Targeting Thyroid Hormone Receptor Beta in Triple Negative Breast Cancer"

Article Title: Targeting Thyroid Hormone Receptor Beta in Triple Negative Breast Cancer

Journal: Breast cancer research and treatment

doi: 10.1007/s10549-015-3354-y

Knockdown of TRβ enhances resistance to docetaxel and doxorubicin A, B . HCC2185 and HCC202 cells (EV and shTRβ) were treated with DOC, DOX or CIS for 3 days and IC50 values were calculated using MTT growth assays performed in triplicate. C, D, E. HCC2185, HCC202 and MDA-MB-453 cells were treated with DOC 1 or 5 nM (T1 and T5, respectively), DOX 10 nM or 100 nM (D10 or D100, respectively) or CIS 0.1 uM or 1 uM (C0.1 or C1, respectively) for 2 months, and endogenous TRβ protein levels were measured using western blot. GAPDH or RhoGDIα levels were used as loading controls. F, G . HCC2185 and HCC202 cells (EV and shTRβ) were treated with DOC 1 nM (T), DOX 100 nM (D) and CIS 1 uM (C) for 4 days, and then western blots were performed for TRβ, cleaved PARP, PARP, cleaved caspase 3 and caspase 3 expression. GAPDH was used as a loading control.
Figure Legend Snippet: Knockdown of TRβ enhances resistance to docetaxel and doxorubicin A, B . HCC2185 and HCC202 cells (EV and shTRβ) were treated with DOC, DOX or CIS for 3 days and IC50 values were calculated using MTT growth assays performed in triplicate. C, D, E. HCC2185, HCC202 and MDA-MB-453 cells were treated with DOC 1 or 5 nM (T1 and T5, respectively), DOX 10 nM or 100 nM (D10 or D100, respectively) or CIS 0.1 uM or 1 uM (C0.1 or C1, respectively) for 2 months, and endogenous TRβ protein levels were measured using western blot. GAPDH or RhoGDIα levels were used as loading controls. F, G . HCC2185 and HCC202 cells (EV and shTRβ) were treated with DOC 1 nM (T), DOX 100 nM (D) and CIS 1 uM (C) for 4 days, and then western blots were performed for TRβ, cleaved PARP, PARP, cleaved caspase 3 and caspase 3 expression. GAPDH was used as a loading control.

Techniques Used: MTT Assay, Multiple Displacement Amplification, Western Blot, Expressing

45) Product Images from "Drug discovery using clinical outcome-based Connectivity Mapping: application to ovarian cancer"

Article Title: Drug discovery using clinical outcome-based Connectivity Mapping: application to ovarian cancer

Journal: BMC Genomics

doi: 10.1186/s12864-016-3149-5

Drug dose response curves for five compounds for ovarian cancer cell line A2780: mitoxantrone, podophyllotoxin, wortmannin, doxorubicin, and 17-AAG
Figure Legend Snippet: Drug dose response curves for five compounds for ovarian cancer cell line A2780: mitoxantrone, podophyllotoxin, wortmannin, doxorubicin, and 17-AAG

Techniques Used:

46) Product Images from "Facile Tumor Spheroids Formation in Large Quantity with Controllable Size and High Uniformity"

Article Title: Facile Tumor Spheroids Formation in Large Quantity with Controllable Size and High Uniformity

Journal: Scientific Reports

doi: 10.1038/s41598-018-25203-3

The drug effect on HCT116 tumor spheroids by APH assay. Similar size spheroids (diameter ~500 µm) were treated with different concentrations of Paclitaxel and Doxorubicin for 72 h, and ( A ) shows a typical controlled spheroid, while ( B ) shows a spheroid that was treated by 500 nM Paclitaxel for 72 h. More detailed images can be found in Fig. S10 . Drug effects of Paclitaxel ( C ) and Doxorubicin ( D ) in spheroids cultures, with comparison to monolayer cell cultures. Dose-response curves were plotted exponentially. Scale bars = 200 µm.
Figure Legend Snippet: The drug effect on HCT116 tumor spheroids by APH assay. Similar size spheroids (diameter ~500 µm) were treated with different concentrations of Paclitaxel and Doxorubicin for 72 h, and ( A ) shows a typical controlled spheroid, while ( B ) shows a spheroid that was treated by 500 nM Paclitaxel for 72 h. More detailed images can be found in Fig. S10 . Drug effects of Paclitaxel ( C ) and Doxorubicin ( D ) in spheroids cultures, with comparison to monolayer cell cultures. Dose-response curves were plotted exponentially. Scale bars = 200 µm.

Techniques Used:

47) Product Images from "BIM is the primary mediator of MYC-induced apoptosis in multiple solid tissues"

Article Title: BIM is the primary mediator of MYC-induced apoptosis in multiple solid tissues

Journal: Cell reports

doi: 10.1016/j.celrep.2014.07.057

(A) Representative images of TUNEL staining of apoptotic cells in tissues of mice of the indicated genotypes treated daily with Tamoxifen (50mg/kg) for 3 days and Doxorubicin (10mg/kg) on the 3rd day. Scale bar = 50μm. (B) Quantification (Mean,
Figure Legend Snippet: (A) Representative images of TUNEL staining of apoptotic cells in tissues of mice of the indicated genotypes treated daily with Tamoxifen (50mg/kg) for 3 days and Doxorubicin (10mg/kg) on the 3rd day. Scale bar = 50μm. (B) Quantification (Mean,

Techniques Used: TUNEL Assay, Staining, Mouse Assay

48) Product Images from "Mechanism of drug release from double-walled PDLLA(PLGA) microspheres"

Article Title: Mechanism of drug release from double-walled PDLLA(PLGA) microspheres

Journal: Biomaterials

doi: 10.1016/j.biomaterials.2013.02.015

In vitro release of doxorubicin from double-walled PDLLA(PLGA) microspheres.
Figure Legend Snippet: In vitro release of doxorubicin from double-walled PDLLA(PLGA) microspheres.

Techniques Used: In Vitro

Schematic illustration of the proposed mechanism for the release of doxorubicin from double-walled PDLLA(PLGA) microspheres. PLGA core and PDLLA shell layer are represented by light and dark brown respectively, while doxorubicin molecules are represented by green dots. (a) and (b) show the degradation process of formulations A and B microspheres respectively. Stage I: Initial microspheres before degradation. Stage II: Water penetration into the microspheres and pore formation on the PDLLA shell layer. Stage III: Increase in the number and size of pores on the PDLLA shell layer, and rapid erosion of the PLGA core. Stage IV: Release of doxorubicin into the aqueous medium through pores and/or cavities of the microspheres.
Figure Legend Snippet: Schematic illustration of the proposed mechanism for the release of doxorubicin from double-walled PDLLA(PLGA) microspheres. PLGA core and PDLLA shell layer are represented by light and dark brown respectively, while doxorubicin molecules are represented by green dots. (a) and (b) show the degradation process of formulations A and B microspheres respectively. Stage I: Initial microspheres before degradation. Stage II: Water penetration into the microspheres and pore formation on the PDLLA shell layer. Stage III: Increase in the number and size of pores on the PDLLA shell layer, and rapid erosion of the PLGA core. Stage IV: Release of doxorubicin into the aqueous medium through pores and/or cavities of the microspheres.

Techniques Used:

Laser scanning confocal images and fluorescence intensity profiles depicting the distribution of doxorubicin in the double-walled PDLLA(PLGA) microspheres during the initial stage of the degradation process (0 to 26 days). (a(i)) and (a(ii)) are images of initial microspheres before degradation, (a(iii)) and (a(iv)) 12 days, and (a(v)) and (a(vi)) 26 days after degradation. Scale bar = 50 µm. (b) and (c) are the fluorescence intensity profiles of doxorubicin in representative microspheres of formulations A and B respectively. The inserts are the confocal images captured at the centerline of the microspheres, and the profile is based on the radial average fluorescence intensity from the center of the microsphere.
Figure Legend Snippet: Laser scanning confocal images and fluorescence intensity profiles depicting the distribution of doxorubicin in the double-walled PDLLA(PLGA) microspheres during the initial stage of the degradation process (0 to 26 days). (a(i)) and (a(ii)) are images of initial microspheres before degradation, (a(iii)) and (a(iv)) 12 days, and (a(v)) and (a(vi)) 26 days after degradation. Scale bar = 50 µm. (b) and (c) are the fluorescence intensity profiles of doxorubicin in representative microspheres of formulations A and B respectively. The inserts are the confocal images captured at the centerline of the microspheres, and the profile is based on the radial average fluorescence intensity from the center of the microsphere.

Techniques Used: Fluorescence

49) Product Images from "Biomimetic cellular vectors for enhancing drug delivery to the lungs"

Article Title: Biomimetic cellular vectors for enhancing drug delivery to the lungs

Journal: Scientific Reports

doi: 10.1038/s41598-019-55909-x

Effect of DOX loading in CELVEC performance. ( A ) Flow cytometry dot plot depicting PS on CELVEC (blue) and DOX@CELVEC (green) surface 4 h post-generation. ( B ) Quantitative assessment of flow cytometry dot plot data exhibiting DOX and Annexin V positive cells using gates established in (A). ( C ) Cytotoxic evaluation of murine macrophage cells following electroporation (CELVEC, blue) and electroporation supplemented with DOX (DOX@CELVEC, green) to create DOX@CELVEC. Neutral red uptake was employed to evaluate cellular viability and proliferation over 72 h. Doxorubicin loading was performed at 20 mg/mL. Values normalized to untreated murine macrophages (CTRL). ( D ) Quantification of CELVEC adhered to TNF-α-activated HUVEC following 30 min of in vivo -like flow conditions of 0.1 dyn/cm 2 . ( E ) Representative fluorescent microscope images used for ( D,E ) depicting CELVEC adhesion following 30 min. of flow. Scale bar, 100 μm. The data is plotted as the mean ± SEM. ***p
Figure Legend Snippet: Effect of DOX loading in CELVEC performance. ( A ) Flow cytometry dot plot depicting PS on CELVEC (blue) and DOX@CELVEC (green) surface 4 h post-generation. ( B ) Quantitative assessment of flow cytometry dot plot data exhibiting DOX and Annexin V positive cells using gates established in (A). ( C ) Cytotoxic evaluation of murine macrophage cells following electroporation (CELVEC, blue) and electroporation supplemented with DOX (DOX@CELVEC, green) to create DOX@CELVEC. Neutral red uptake was employed to evaluate cellular viability and proliferation over 72 h. Doxorubicin loading was performed at 20 mg/mL. Values normalized to untreated murine macrophages (CTRL). ( D ) Quantification of CELVEC adhered to TNF-α-activated HUVEC following 30 min of in vivo -like flow conditions of 0.1 dyn/cm 2 . ( E ) Representative fluorescent microscope images used for ( D,E ) depicting CELVEC adhesion following 30 min. of flow. Scale bar, 100 μm. The data is plotted as the mean ± SEM. ***p

Techniques Used: Flow Cytometry, Cytometry, Electroporation, In Vivo, Microscopy

CELVEC as a drug delivery vehicle. ( A ) Loading of doxorubicin (DOX) into CELVEC as a function of initial DOX concentration used. ( B ) Release of DOX from macrophages over 24 h when loading was performed passively (left) or supplemented with electroporation (right). Inset graphs depict DOX release over 6 h as determined using a one-phase association ordinary fit line. Dotted black line designated 50% release of payload. ( C ) Cellular viability of human MDA-231 triple negative breast cancer cells following treatment with free DOX and DOX-loaded CELVEC at low (325 nM) and high (975 nM) dosages. The data is plotted as the mean ± SEM. *p
Figure Legend Snippet: CELVEC as a drug delivery vehicle. ( A ) Loading of doxorubicin (DOX) into CELVEC as a function of initial DOX concentration used. ( B ) Release of DOX from macrophages over 24 h when loading was performed passively (left) or supplemented with electroporation (right). Inset graphs depict DOX release over 6 h as determined using a one-phase association ordinary fit line. Dotted black line designated 50% release of payload. ( C ) Cellular viability of human MDA-231 triple negative breast cancer cells following treatment with free DOX and DOX-loaded CELVEC at low (325 nM) and high (975 nM) dosages. The data is plotted as the mean ± SEM. *p

Techniques Used: Concentration Assay, Electroporation, Multiple Displacement Amplification

Related Articles

Centrifugation:

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Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn,MA). .. To convert the drug into the hydrophobic form, doxorubicin hydrochloridewas neutralized by phosphate buffer solution (0.1 M, pH 8.5) followedby centrifugation.

Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery
Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn, MA). .. To convert the drug into the hydrophobic form, doxorubicin hydrochloride was neutralized by phosphate buffer solution (0.1 M, pH 8.5) followed by centrifugation.

Distillation:

Article Title: Controlled Multi-functionalization Facilitates Targeted Delivery of Nanoparticles to Cancer Cells
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Cytometry:

Article Title: The Role of Cytochromes P450 and Aldo-Keto Reductases in Prognosis of Breast Carcinoma Patients
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Enzyme-linked Immunosorbent Assay:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
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Incubation:

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Article Snippet: .. In combined treatment with doxorubicin (DXR; LC Laboratories, Woburn, MA, USA), the cells were incubated for 24 h at 37°C after transfection at 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA using Lipofectamine RNAiMax reagent, and then treated with various concentrations (0.016–0.5 µM) of DXR as reported previously ( ). .. A total of 6 h after incubation, the medium containing free DXR was changed for fresh medium without DXR, and then incubated for another 18 h at 37°C.

Article Title: The Role of Cytochromes P450 and Aldo-Keto Reductases in Prognosis of Breast Carcinoma Patients
Article Snippet: Next day (after 18 hours), culture medium was replaced by the culture medium without drugs (control) or with 100 nM paclitaxel (PCT) or 30 μM adriamycin (LC Laboratories, Woburn, MA). .. Fixed cells were washed with phosphate-buffered saline, incubated with 40 μg/mL propidium iodide and 100 μg/mL RNase in phosphate-buffered saline, and cell cycle was analyzed using flow cytometer FACSVersa (Becton, Dickinson and Company, Franklin Lakes, NJ).

Proliferation Assay:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
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Expressing:

Article Title: The Role of Cytochromes P450 and Aldo-Keto Reductases in Prognosis of Breast Carcinoma Patients
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Modification:

Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery
Article Snippet: Dulbecco’s phosphate-buffered saline(PBS), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT), Dulbecco’s modified Eagle’s medium (DMEM), andfetal bovine serum (FBS) were purchased from Invitrogen (Carlsbad,CA). .. Doxorubicin hydrochloride was obtained from LC laboratories (Woburn,MA).

Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery
Article Snippet: Dulbecco’s phosphate-buffered saline (PBS), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Dulbecco’s modified Eagle’s medium (DMEM), and fetal bovine serum (FBS) were purchased from Invitrogen (Carlsbad, CA). .. Doxorubicin hydrochloride was obtained from LC laboratories (Woburn, MA).

Derivative Assay:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
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Transfection:

Article Title: Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA
Article Snippet: .. In combined treatment with doxorubicin (DXR; LC Laboratories, Woburn, MA, USA), the cells were incubated for 24 h at 37°C after transfection at 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA using Lipofectamine RNAiMax reagent, and then treated with various concentrations (0.016–0.5 µM) of DXR as reported previously ( ). .. A total of 6 h after incubation, the medium containing free DXR was changed for fresh medium without DXR, and then incubated for another 18 h at 37°C.

Serial Dilution:

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling
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Cell Culture:

Article Title: Label-Free Recognition of Drug Resistance via Impedimetric Screening of Breast Cancer Cells
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Inhibition:

Article Title: Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA
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Droplet Countercurrent Chromatography:

Article Title: Controlled Multi-functionalization Facilitates Targeted Delivery of Nanoparticles to Cancer Cells
Article Snippet: 2,000 Da), p -toluenesulfonyl chloride, sodium azide, dimethylformamide (DMF, 99.8%), 4-(dimethyl amino) pyridine (DMAP, 99%), 1,3-dicyclohexyl carbodiimide (DCC, 99%), hydrogen tetrachloroaurate (III) trihydrate (HAuCl4 ·3H2 O, 99.9%), triethylamine (99.5%), thioctic acid (98%), N-hydroxysuccinamide (NHS, 99%), p-nitrophenyl chloroformate (96%), hydrazine monohydrate (98%), 1,2 dichloroethane, sodium methoxide, and 4-biphenyl-carboxylic acid, Neu5Ac were purchased from Carbosynth LLC and lithium aluminium hydride (LiAlH4, 95%) was obtained from Aldrich. .. Doxorubicin hydrochloride was purchased from LC Laboratories.

Recombinant:

Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery
Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn, MA). .. Methods used for the synthesis of recombinant silk-elastin-like protein polymers (SE8Y, S2E8Y and S4E8Y) with silk to elastin ratios at 1:8, 1:4, and 1:2, and molecular weights of 55.7, 53.0, and 47.8 kDa, respectively, have been described previously.

Molecular Weight:

Article Title: Controlled Multi-functionalization Facilitates Targeted Delivery of Nanoparticles to Cancer Cells
Article Snippet: Polyethylene glycol (PEG, number average molecular weight, M n ~2,000 Da), polyethylene glycol monomethyl ether ( M n ca. .. Doxorubicin hydrochloride was purchased from LC Laboratories.

MTT Assay:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
Article Snippet: Doxorubicin (D-4000) was purchased from LC Laboratories (Woburn, MA). .. CellEvent Caspase-3/7 Green Detection Reagent, Vybrant MTT cell proliferation assay kit and Annexin V-FITC/PI apoptosis detection kit were obtained from Molecular Probes (Eugene, OR).

Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery
Article Snippet: Dulbecco’s phosphate-buffered saline (PBS), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Dulbecco’s modified Eagle’s medium (DMEM), and fetal bovine serum (FBS) were purchased from Invitrogen (Carlsbad, CA). .. Doxorubicin hydrochloride was obtained from LC laboratories (Woburn, MA).

Multiple Displacement Amplification:

Article Title: Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA
Article Snippet: Cell growth inhibition MCF-7, MDA-MB-231 and HeLa cells were seeded in 96-well plates at a density of 2×104 cells per well 24 h prior to transfection. .. In combined treatment with doxorubicin (DXR; LC Laboratories, Woburn, MA, USA), the cells were incubated for 24 h at 37°C after transfection at 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA using Lipofectamine RNAiMax reagent, and then treated with various concentrations (0.016–0.5 µM) of DXR as reported previously ( ).

Isolation:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
Article Snippet: Doxorubicin (D-4000) was purchased from LC Laboratories (Woburn, MA). .. Ginger derived nanoparticles isolation and purification.

Flow Cytometry:

Article Title: The Role of Cytochromes P450 and Aldo-Keto Reductases in Prognosis of Breast Carcinoma Patients
Article Snippet: Paragraph title: Cell Proliferation Assessment by Flow Cytometry ... Next day (after 18 hours), culture medium was replaced by the culture medium without drugs (control) or with 100 nM paclitaxel (PCT) or 30 μM adriamycin (LC Laboratories, Woburn, MA).

Purification:

Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy
Article Snippet: Doxorubicin (D-4000) was purchased from LC Laboratories (Woburn, MA). .. Ginger derived nanoparticles isolation and purification.

Chromatin Immunoprecipitation:

Article Title: Label-Free Recognition of Drug Resistance via Impedimetric Screening of Breast Cancer Cells
Article Snippet: MCF-7 DOX cells were cultured in the presence of 1 µg/ml doxorubicin (LC Laboratories, USA) in order to maintain the drug-resistance phenotype. .. For each electrode chip, one PMMA well was attached on it with polydimethylsiloxane (PDMS) ( ).

Software:

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling
Article Snippet: The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr. .. Data were normalized to an untreated control well and graphed using GraphPad Prism software, and half maximal inhibitory concentration (IC50 ) values were calculated from the dose-response curve as the concentration of doxorubicin or cisplatin that produced a 50% decrease in the mean cell viability relative to untreated control wells.

Real-time Polymerase Chain Reaction:

Article Title: The Role of Cytochromes P450 and Aldo-Keto Reductases in Prognosis of Breast Carcinoma Patients
Article Snippet: Next day (after 18 hours), culture medium was replaced by the culture medium without drugs (control) or with 100 nM paclitaxel (PCT) or 30 μM adriamycin (LC Laboratories, Woburn, MA). .. CYP3A4 and AKR1C2 expression was monitored by qPCR and immunoblotting in parallel samples 48 hours after exposure to drugs.

Column Chromatography:

Article Title: Controlled Multi-functionalization Facilitates Targeted Delivery of Nanoparticles to Cancer Cells
Article Snippet: Doxorubicin hydrochloride was purchased from LC Laboratories. .. Column chromatography was performed on 70–230-mesh silica gel.

CCK-8 Assay:

Article Title: Evaluation of in vitro and in vivo therapeutic antitumor efficacy of transduction of polo-like kinase 1 and heat shock transcription factor 1 small interfering RNA
Article Snippet: In combined treatment with doxorubicin (DXR; LC Laboratories, Woburn, MA, USA), the cells were incubated for 24 h at 37°C after transfection at 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA using Lipofectamine RNAiMax reagent, and then treated with various concentrations (0.016–0.5 µM) of DXR as reported previously ( ). .. In combined treatment with doxorubicin (DXR; LC Laboratories, Woburn, MA, USA), the cells were incubated for 24 h at 37°C after transfection at 50 nM Cont siRNA, PLK1 siRNA or HSF1 siRNA using Lipofectamine RNAiMax reagent, and then treated with various concentrations (0.016–0.5 µM) of DXR as reported previously ( ).

Produced:

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling
Article Snippet: The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr. .. Data were normalized to an untreated control well and graphed using GraphPad Prism software, and half maximal inhibitory concentration (IC50 ) values were calculated from the dose-response curve as the concentration of doxorubicin or cisplatin that produced a 50% decrease in the mean cell viability relative to untreated control wells.

Concentration Assay:

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling
Article Snippet: .. The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr. .. Cell viability was then determined using the CellTiter-Glo Luminescent Cell Viability assay (Promega).

Cell Viability Assay:

Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling
Article Snippet: The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr. .. Cell viability was then determined using the CellTiter-Glo Luminescent Cell Viability assay (Promega).

other:

Article Title: Analysis of redox and apoptotic effects of anthracyclines to delineate a cardioprotective strategy
Article Snippet: Doxorubicin was purchased from LC Laboratories.

Article Title: Doxorubicin Blocks Cardiomyocyte Autophagic Flux by Inhibiting Lysosome Acidification
Article Snippet: Doxorubicin was purchased from LC laboratories.

Article Title: Cyclodextrin-Based Magnetic Nanoparticles for Cancer Therapy
Article Snippet: Materials and Methods All of the chemical reagents were purchased from Sigma-Aldrich (Poznan, Poland), except for the dopamine hydrochloride (Alfa Aesar, Gdansk, Poland) and doxorubicin hydrochloride (LC Laboratories, Boston, MA, USA).

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  • 88
    LC Laboratories doxorubicin hcl
    Equilibration adsorption of <t>doxorubicin</t> to silk films Doxorubicin binding to (A, C and E) low crystallinity and (B, D and F) high crystallinity unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) silk films. Data represent the mean ± S.D. from three independent experiments, N.D.: no differences between groups.
    Doxorubicin Hcl, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin hcl/product/LC Laboratories
    Average 88 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    doxorubicin hcl - by Bioz Stars, 2020-04
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    93
    LC Laboratories doxorubicin hydrochloride
    DLS size distributionprofiles for <t>doxorubicin</t> encapsulated SE8Y(S1/Dox) nanoparticles in phosphate buffer saline with 10% FBS at37 °C over time.
    Doxorubicin Hydrochloride, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin hydrochloride/product/LC Laboratories
    Average 93 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    doxorubicin hydrochloride - by Bioz Stars, 2020-04
    93/100 stars
      Buy from Supplier

    Image Search Results


    Equilibration adsorption of doxorubicin to silk films Doxorubicin binding to (A, C and E) low crystallinity and (B, D and F) high crystallinity unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) silk films. Data represent the mean ± S.D. from three independent experiments, N.D.: no differences between groups.

    Journal: Journal of controlled release : official journal of the Controlled Release Society

    Article Title: Modulation of Vincristine and Doxorubicin Binding and Release from Silk Films

    doi: 10.1016/j.jconrel.2015.10.035

    Figure Lengend Snippet: Equilibration adsorption of doxorubicin to silk films Doxorubicin binding to (A, C and E) low crystallinity and (B, D and F) high crystallinity unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) silk films. Data represent the mean ± S.D. from three independent experiments, N.D.: no differences between groups.

    Article Snippet: Doxorubicin·HCl and vincristine sodium sulfate were purchased from LC Laboratories (Woburn, MA).

    Techniques: Adsorption, Binding Assay, Modification, Introduce

    Doxorubicin and vincristine binding to low crystallinity silk films under varying solution conditions Effect of (A and B) polysorbate 80, (C and D) pH and (E and F) ionic strength on (A, C and E) doxorubicin and (B, D and F) vincristine binding to unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) silk films. Data represent the mean ± S.D. from three independent experiments each with three separate samples. * p

    Journal: Journal of controlled release : official journal of the Controlled Release Society

    Article Title: Modulation of Vincristine and Doxorubicin Binding and Release from Silk Films

    doi: 10.1016/j.jconrel.2015.10.035

    Figure Lengend Snippet: Doxorubicin and vincristine binding to low crystallinity silk films under varying solution conditions Effect of (A and B) polysorbate 80, (C and D) pH and (E and F) ionic strength on (A, C and E) doxorubicin and (B, D and F) vincristine binding to unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) silk films. Data represent the mean ± S.D. from three independent experiments each with three separate samples. * p

    Article Snippet: Doxorubicin·HCl and vincristine sodium sulfate were purchased from LC Laboratories (Woburn, MA).

    Techniques: Binding Assay, Modification, Introduce

    Kinetic adsorption of doxorubicin on silk films Doxorubicin binding to (A and D) unmodified (silk), (B and E) carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and (C and F) sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) low crystallinity (white symbols) and high crystallinity (grey symbols) silk films. The experiments were performed for (A–C) one week (low crystallinity) or two weeks (high crystallinity); (D–F) shows the data for the first 8 hours. Data represent the mean ± S.D. from three separate samples.

    Journal: Journal of controlled release : official journal of the Controlled Release Society

    Article Title: Modulation of Vincristine and Doxorubicin Binding and Release from Silk Films

    doi: 10.1016/j.jconrel.2015.10.035

    Figure Lengend Snippet: Kinetic adsorption of doxorubicin on silk films Doxorubicin binding to (A and D) unmodified (silk), (B and E) carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and (C and F) sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) low crystallinity (white symbols) and high crystallinity (grey symbols) silk films. The experiments were performed for (A–C) one week (low crystallinity) or two weeks (high crystallinity); (D–F) shows the data for the first 8 hours. Data represent the mean ± S.D. from three separate samples.

    Article Snippet: Doxorubicin·HCl and vincristine sodium sulfate were purchased from LC Laboratories (Woburn, MA).

    Techniques: Adsorption, Binding Assay, Modification, Introduce

    Drug loading of silk films (A) Doxorubicin and (B) vincristine loading in unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) low crystallinity and high crystallinity silk films. Data represent the mean ± S.D. from three independent experiments each with three separate samples. ** p

    Journal: Journal of controlled release : official journal of the Controlled Release Society

    Article Title: Modulation of Vincristine and Doxorubicin Binding and Release from Silk Films

    doi: 10.1016/j.jconrel.2015.10.035

    Figure Lengend Snippet: Drug loading of silk films (A) Doxorubicin and (B) vincristine loading in unmodified (silk), carboxylate (silk modified via diazonium coupling chemistry to increase carboxylate content) and sulfonate (silk modified via diazonium coupling chemistry to introduce sulfonate groups) low crystallinity and high crystallinity silk films. Data represent the mean ± S.D. from three independent experiments each with three separate samples. ** p

    Article Snippet: Doxorubicin·HCl and vincristine sodium sulfate were purchased from LC Laboratories (Woburn, MA).

    Techniques: Modification, Introduce

    Ginger-derived nanovectors (GDNVs) can be used as a drug carrier and load therapeutic agent-doxorubicin (Dox) efficiency. ( a ) Loading efficiency of Dox in GDNVs was measured. 200 μg of Dox solution was added into the ginger lipid film (the lipid

    Journal: Molecular Therapy

    Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy

    doi: 10.1038/mt.2016.159

    Figure Lengend Snippet: Ginger-derived nanovectors (GDNVs) can be used as a drug carrier and load therapeutic agent-doxorubicin (Dox) efficiency. ( a ) Loading efficiency of Dox in GDNVs was measured. 200 μg of Dox solution was added into the ginger lipid film (the lipid

    Article Snippet: Doxorubicin (D-4000) was purchased from LC Laboratories (Woburn, MA).

    Techniques: Derivative Assay

    Evaluation the apoptosis in Colon-26 cells induced by free doxorubicin (Dox) and Dox-GDNVs using Annexin V-FITC/PI staining and ECIS technology. ( a ) Control group. ( b ) Free Dox group. ( c ) Dox-GDNVs group. Cells were treated with three different Dox concentrations

    Journal: Molecular Therapy

    Article Title: Edible Ginger-derived Nano-lipids Loaded with Doxorubicin as a Novel Drug-delivery Approach for Colon Cancer Therapy

    doi: 10.1038/mt.2016.159

    Figure Lengend Snippet: Evaluation the apoptosis in Colon-26 cells induced by free doxorubicin (Dox) and Dox-GDNVs using Annexin V-FITC/PI staining and ECIS technology. ( a ) Control group. ( b ) Free Dox group. ( c ) Dox-GDNVs group. Cells were treated with three different Dox concentrations

    Article Snippet: Doxorubicin (D-4000) was purchased from LC Laboratories (Woburn, MA).

    Techniques: Staining, Electric Cell-substrate Impedance Sensing

    Anoikis-resistant OS cells show resistance to standard OS chemotherapies. Dose-response curves for cells grown under AI or adherent conditions treated with doxorubicin (top panel) or cisplatin (bottom panel) in a set of serial dilutions for 72 hours. Cell viability was determined as a percentage of the untreated control (0 μM doxorubicin or cisplatin).

    Journal: Journal of Translational Medicine

    Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling

    doi: 10.1186/s12967-015-0466-4

    Figure Lengend Snippet: Anoikis-resistant OS cells show resistance to standard OS chemotherapies. Dose-response curves for cells grown under AI or adherent conditions treated with doxorubicin (top panel) or cisplatin (bottom panel) in a set of serial dilutions for 72 hours. Cell viability was determined as a percentage of the untreated control (0 μM doxorubicin or cisplatin).

    Article Snippet: The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr.

    Techniques:

    5-azaC treatment inhibits anchorage-independent OS cell growth while sensitizing to doxorubicin. A/B : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug and allowed to grow for 4 days. 5-azaC treatment decreased the cells ability to form spheres (A) and resulted in a significant decrease in cell viability (B) . C/D : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug. 24 hours later the cells were treated with one concentration from a serial dilution of doxorubicin, with cell viability being measured after an additional 72 hours. 5-azaC treatment resulted in a left-shift in the doxorubicin dose-response curve (C) and a significant decrease in the percent IC 50 relative to vehicle alone (D) . Asterisks indicate statistical significance (*p

    Journal: Journal of Translational Medicine

    Article Title: Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling

    doi: 10.1186/s12967-015-0466-4

    Figure Lengend Snippet: 5-azaC treatment inhibits anchorage-independent OS cell growth while sensitizing to doxorubicin. A/B : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug and allowed to grow for 4 days. 5-azaC treatment decreased the cells ability to form spheres (A) and resulted in a significant decrease in cell viability (B) . C/D : Adherent mHOS cells were treated with either 2 μM 5-azaC or vehicle alone for 24 hours before being plated in AI conditions in the absence of drug. 24 hours later the cells were treated with one concentration from a serial dilution of doxorubicin, with cell viability being measured after an additional 72 hours. 5-azaC treatment resulted in a left-shift in the doxorubicin dose-response curve (C) and a significant decrease in the percent IC 50 relative to vehicle alone (D) . Asterisks indicate statistical significance (*p

    Article Snippet: The cells were then exposed to one concentration from a serial dilution of doxorubicin (0-10 μM; LC Labs) or cisplatin (0-100 μM; Sigma) for 72 hr.

    Techniques: Concentration Assay, Serial Dilution

    DLS size distributionprofiles for doxorubicin encapsulated SE8Y(S1/Dox) nanoparticles in phosphate buffer saline with 10% FBS at37 °C over time.

    Journal: Biomacromolecules

    Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery

    doi: 10.1021/bm4017594

    Figure Lengend Snippet: DLS size distributionprofiles for doxorubicin encapsulated SE8Y(S1/Dox) nanoparticles in phosphate buffer saline with 10% FBS at37 °C over time.

    Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn,MA).

    Techniques:

    (a) Cytotoxicity of the SE8Y (S1), S2E8Y (S2), and S4E8Y(S4) proteinpolymers against Hela cells. (b) In vitro cytotoxicity of SE8Y/Dox(S1/Dox), S2E8Y/Dox (S2/Dox), and S4E8Y/Dox (S4/Dox) complexes andfree doxorubicin against HeLa cells. (c) IC 50 values

    Journal: Biomacromolecules

    Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery

    doi: 10.1021/bm4017594

    Figure Lengend Snippet: (a) Cytotoxicity of the SE8Y (S1), S2E8Y (S2), and S4E8Y(S4) proteinpolymers against Hela cells. (b) In vitro cytotoxicity of SE8Y/Dox(S1/Dox), S2E8Y/Dox (S2/Dox), and S4E8Y/Dox (S4/Dox) complexes andfree doxorubicin against HeLa cells. (c) IC 50 values

    Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn,MA).

    Techniques: In Vitro

    Characterizationof doxorubicin-encapsulated nanoparticles. (a)Sizes of SE8Y/Dox, S2E8Y/Dox, and S4E8Y/Dox complexes at 25 °C(gray bar) and 37 °C (black bar) with respective protein solutionsas controls (white bar). (b) Turbidity profiles

    Journal: Biomacromolecules

    Article Title: Hydrophobic Drug-Triggered Self-Assembly of Nanoparticles from Silk-Elastin-Like Protein Polymers for Drug Delivery

    doi: 10.1021/bm4017594

    Figure Lengend Snippet: Characterizationof doxorubicin-encapsulated nanoparticles. (a)Sizes of SE8Y/Dox, S2E8Y/Dox, and S4E8Y/Dox complexes at 25 °C(gray bar) and 37 °C (black bar) with respective protein solutionsas controls (white bar). (b) Turbidity profiles

    Article Snippet: Doxorubicin hydrochloride was obtained from LC laboratories (Woburn,MA).

    Techniques: