doxorubicin hydrochloride Cayman Chemical Search Results


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  • 99
    Tocris doxorubicin
    Doxorubicin, supplied by Tocris, used in various techniques. Bioz Stars score: 99/100, based on 97 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin/product/Tocris
    Average 99 stars, based on 97 article reviews
    Price from $9.99 to $1999.99
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    95
    Cayman Chemical doxorubicin
    WDR23 overexpression enhances chemotherapy toxicity. ( A-C ) Cells overexpressing GFP:WDR23 isoform 1 (pink) or GFP:WDR23 isoform 2 (orange) are more sensitive to increasing concentrations of ( A ) etoposide (25uM n = 12 each, 50um n = 8 each, 75um n = 8 each), ( B ) <t>doxorubicin</t> (1uM n = 12 each, 2uM n = 8 each), or ( C ) cisplatin (50uM n = 12 each, 75uM n = 8 each, 100uM n = 8 each) as compared to cells expressing GFP alone (black). ( D,E ) The percentage of cells carrying DNA double strand breaks (DSB), as indicated by dual phospho-H2Ax and phospho-ATM staining, is increased when WDR23 isoform 1 or WDR23 isoform 2 is overexpressed (Control n = 3, Iso 1 n = 3, Iso 2 n = 3) and ( E ) enhances DSB incidence following etoposide treatment (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). ( F ) Cellular apoptosis (Annexin V positive) is increased in cells overexpressing WDR23 isoform 1 or WDR23 isoform 2 as compared to control cells overexpressing GFP alone (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). Data are mean ± s.e.m.; one-tailed t -test relative to control GFP overexpression for each treatment condition. * P
    Doxorubicin, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 95/100, based on 83 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin/product/Cayman Chemical
    Average 95 stars, based on 83 article reviews
    Price from $9.99 to $1999.99
    doxorubicin - by Bioz Stars, 2020-04
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    92
    Cayman Chemical doxorubicin hydrochloride dox hcl
    Light templated <t>doxorubicin</t> delivery in vitro. Patterned light (365 nm, 15–17 mW/cm 2 ) activation of 1 (300 μM) and cellular uptake of DOX ( red ).
    Doxorubicin Hydrochloride Dox Hcl, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin hydrochloride dox hcl/product/Cayman Chemical
    Average 92 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
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    96
    LC Laboratories doxorubicin
    Light templated <t>doxorubicin</t> delivery in vitro. Patterned light (365 nm, 15–17 mW/cm 2 ) activation of 1 (300 μM) and cellular uptake of DOX ( red ).
    Doxorubicin, supplied by LC Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 245 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin/product/LC Laboratories
    Average 96 stars, based on 245 article reviews
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    91
    Millipore chemodrug doxorubicin
    Blocking Src's metabolic effect sensitizes cancer cells to pro-oxidant chemotherapy A, B. Src inhibitors and <t>chemodrug</t> <t>Doxorubicin</t> (Dox) show additive/synergistic effects on ROS induction and suppression of cell growth/viability. 4T1 cells were treated with Dox (1 μg/ml) and Src inhibitors SA and SU (1 μM each). ROS levels (A) and cell growth and viability (B) were subsequently determined. C, D. Expression of PDHA1 Y289F sensitizes cells to pro-oxidant. 4T1 cells transduced with WT or Y289F PDHA1 were treated with vehicle (DMSO) or Dox, followed by measurement of ROS levels (C) and cell growth and survival (D). Error bars represent S.D. *p
    Chemodrug Doxorubicin, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/chemodrug doxorubicin/product/Millipore
    Average 91 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
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    86
    Cayman Chemical cytotoxic agent doxorubicin
    Blocking Src's metabolic effect sensitizes cancer cells to pro-oxidant chemotherapy A, B. Src inhibitors and <t>chemodrug</t> <t>Doxorubicin</t> (Dox) show additive/synergistic effects on ROS induction and suppression of cell growth/viability. 4T1 cells were treated with Dox (1 μg/ml) and Src inhibitors SA and SU (1 μM each). ROS levels (A) and cell growth and viability (B) were subsequently determined. C, D. Expression of PDHA1 Y289F sensitizes cells to pro-oxidant. 4T1 cells transduced with WT or Y289F PDHA1 were treated with vehicle (DMSO) or Dox, followed by measurement of ROS levels (C) and cell growth and survival (D). Error bars represent S.D. *p
    Cytotoxic Agent Doxorubicin, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 86/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cytotoxic agent doxorubicin/product/Cayman Chemical
    Average 86 stars, based on 3 article reviews
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    97
    Santa Cruz Biotechnology doxorubicin
    Pharmacological or genetic inhibition of DNM1L blocks mitochondrial fission and apoptosis induced by liensinine in combination with <t>doxorubicin.</t> ( A ) MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence
    Doxorubicin, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 82 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin/product/Santa Cruz Biotechnology
    Average 97 stars, based on 82 article reviews
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    92
    Cayman Chemical doxorubicin dox
    Pharmacological or genetic inhibition of DNM1L blocks mitochondrial fission and apoptosis induced by liensinine in combination with <t>doxorubicin.</t> ( A ) MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence
    Doxorubicin Dox, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/doxorubicin dox/product/Cayman Chemical
    Average 92 stars, based on 3 article reviews
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    94
    Cayman Chemical epirubicin
    SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or <t>epirubicin</t> (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.
    Epirubicin, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/epirubicin/product/Cayman Chemical
    Average 94 stars, based on 7 article reviews
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    Image Search Results


    WDR23 overexpression enhances chemotherapy toxicity. ( A-C ) Cells overexpressing GFP:WDR23 isoform 1 (pink) or GFP:WDR23 isoform 2 (orange) are more sensitive to increasing concentrations of ( A ) etoposide (25uM n = 12 each, 50um n = 8 each, 75um n = 8 each), ( B ) doxorubicin (1uM n = 12 each, 2uM n = 8 each), or ( C ) cisplatin (50uM n = 12 each, 75uM n = 8 each, 100uM n = 8 each) as compared to cells expressing GFP alone (black). ( D,E ) The percentage of cells carrying DNA double strand breaks (DSB), as indicated by dual phospho-H2Ax and phospho-ATM staining, is increased when WDR23 isoform 1 or WDR23 isoform 2 is overexpressed (Control n = 3, Iso 1 n = 3, Iso 2 n = 3) and ( E ) enhances DSB incidence following etoposide treatment (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). ( F ) Cellular apoptosis (Annexin V positive) is increased in cells overexpressing WDR23 isoform 1 or WDR23 isoform 2 as compared to control cells overexpressing GFP alone (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). Data are mean ± s.e.m.; one-tailed t -test relative to control GFP overexpression for each treatment condition. * P

    Journal: PLoS Genetics

    Article Title: WDR23 regulates NRF2 independently of KEAP1

    doi: 10.1371/journal.pgen.1006762

    Figure Lengend Snippet: WDR23 overexpression enhances chemotherapy toxicity. ( A-C ) Cells overexpressing GFP:WDR23 isoform 1 (pink) or GFP:WDR23 isoform 2 (orange) are more sensitive to increasing concentrations of ( A ) etoposide (25uM n = 12 each, 50um n = 8 each, 75um n = 8 each), ( B ) doxorubicin (1uM n = 12 each, 2uM n = 8 each), or ( C ) cisplatin (50uM n = 12 each, 75uM n = 8 each, 100uM n = 8 each) as compared to cells expressing GFP alone (black). ( D,E ) The percentage of cells carrying DNA double strand breaks (DSB), as indicated by dual phospho-H2Ax and phospho-ATM staining, is increased when WDR23 isoform 1 or WDR23 isoform 2 is overexpressed (Control n = 3, Iso 1 n = 3, Iso 2 n = 3) and ( E ) enhances DSB incidence following etoposide treatment (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). ( F ) Cellular apoptosis (Annexin V positive) is increased in cells overexpressing WDR23 isoform 1 or WDR23 isoform 2 as compared to control cells overexpressing GFP alone (Control n = 3, Iso 1 n = 3, Iso 2 n = 3). Data are mean ± s.e.m.; one-tailed t -test relative to control GFP overexpression for each treatment condition. * P

    Article Snippet: Forty-eight hours post-transfection, cells were treated with the indicated chemical: Etoposide (Cayman), Doxorubicin (Cayman), or Cisplatin (Cayman).

    Techniques: Over Expression, Expressing, Staining, One-tailed Test

    Light templated doxorubicin delivery in vitro. Patterned light (365 nm, 15–17 mW/cm 2 ) activation of 1 (300 μM) and cellular uptake of DOX ( red ).

    Journal: International Journal of Molecular Sciences

    Article Title: Spatiotemporal Control of Doxorubicin Delivery from “Stealth-Like” Prodrug Micelles

    doi: 10.3390/ijms18102033

    Figure Lengend Snippet: Light templated doxorubicin delivery in vitro. Patterned light (365 nm, 15–17 mW/cm 2 ) activation of 1 (300 μM) and cellular uptake of DOX ( red ).

    Article Snippet: Materials and Instruments Doxorubicin hydrochloride (DOX·HCl) was purchased from Cayman Chemical Company (Ann Arbor, MI, USA) and used without further purification.

    Techniques: In Vitro, Activation Assay

    Viability of HeLa cells in vitro treated with doxorubicin pro-drug micelles. ( a ) Cell viability following incubation with varying concentrations (10 nM–100 μM) of free DOX ( black ) and 1 ( red ) in the absence of light; ( b ) Viability of HeLa cells in vitro treated with varying concentrations of 1 and irradiated (365 nm, 15–17 mW/cm 2 ) for up to 1h. Pink line corresponds to photoinduced cytotoxicity.

    Journal: International Journal of Molecular Sciences

    Article Title: Spatiotemporal Control of Doxorubicin Delivery from “Stealth-Like” Prodrug Micelles

    doi: 10.3390/ijms18102033

    Figure Lengend Snippet: Viability of HeLa cells in vitro treated with doxorubicin pro-drug micelles. ( a ) Cell viability following incubation with varying concentrations (10 nM–100 μM) of free DOX ( black ) and 1 ( red ) in the absence of light; ( b ) Viability of HeLa cells in vitro treated with varying concentrations of 1 and irradiated (365 nm, 15–17 mW/cm 2 ) for up to 1h. Pink line corresponds to photoinduced cytotoxicity.

    Article Snippet: Materials and Instruments Doxorubicin hydrochloride (DOX·HCl) was purchased from Cayman Chemical Company (Ann Arbor, MI, USA) and used without further purification.

    Techniques: In Vitro, Incubation, Irradiation

    Characterization of doxorubicin pro-drug micelles and light induced drug release. ( a ) TEM (transmission electron microscopy) image (uranyl acetate stain) of micelles of 1 (300 μM, approx. 0.7 mg/mL); ( b ) Time evolution of the HPLC (high-performance liquid chromatography) spectra of a solution of 1 (100 μM in PBS (phosphate buffered saline)) during photolysis (365 nm, 3–5 mW/cm 2 ). Free DOX (100 μM), dissolved in PBS, was used to confirm clean photolysis of 1 to release “active” DOX. HPLC conditions described in Materials and Methods; ( c ) CMC (critical micelle concentration) determination by light scattering following serial dilution of 1 (100 μM–75 nM) in PBS; ( d ) In vitro DOX release profiles from 1 (300 μM) in PBS. No UV irradiation ( red ), UV irradiation at 9 h ( black ) and free DOX control ( blue ).

    Journal: International Journal of Molecular Sciences

    Article Title: Spatiotemporal Control of Doxorubicin Delivery from “Stealth-Like” Prodrug Micelles

    doi: 10.3390/ijms18102033

    Figure Lengend Snippet: Characterization of doxorubicin pro-drug micelles and light induced drug release. ( a ) TEM (transmission electron microscopy) image (uranyl acetate stain) of micelles of 1 (300 μM, approx. 0.7 mg/mL); ( b ) Time evolution of the HPLC (high-performance liquid chromatography) spectra of a solution of 1 (100 μM in PBS (phosphate buffered saline)) during photolysis (365 nm, 3–5 mW/cm 2 ). Free DOX (100 μM), dissolved in PBS, was used to confirm clean photolysis of 1 to release “active” DOX. HPLC conditions described in Materials and Methods; ( c ) CMC (critical micelle concentration) determination by light scattering following serial dilution of 1 (100 μM–75 nM) in PBS; ( d ) In vitro DOX release profiles from 1 (300 μM) in PBS. No UV irradiation ( red ), UV irradiation at 9 h ( black ) and free DOX control ( blue ).

    Article Snippet: Materials and Instruments Doxorubicin hydrochloride (DOX·HCl) was purchased from Cayman Chemical Company (Ann Arbor, MI, USA) and used without further purification.

    Techniques: Transmission Electron Microscopy, Transmission Assay, Electron Microscopy, Staining, High Performance Liquid Chromatography, Concentration Assay, Serial Dilution, In Vitro, Irradiation

    Light activated doxorubicin pro-drug micelles. ( a ) Doxorubicin- ortho -nitrobenzyl-mPEG 2000 construct, 1 ; ( b ) Self-assembly of 1 in aqueous media to 100 nm PEGylated and DOX (doxorubicin)-rich micelles from which quantitative drug release is triggered by light; ( c ) Light directed DOX release, cell uptake, and cell death.

    Journal: International Journal of Molecular Sciences

    Article Title: Spatiotemporal Control of Doxorubicin Delivery from “Stealth-Like” Prodrug Micelles

    doi: 10.3390/ijms18102033

    Figure Lengend Snippet: Light activated doxorubicin pro-drug micelles. ( a ) Doxorubicin- ortho -nitrobenzyl-mPEG 2000 construct, 1 ; ( b ) Self-assembly of 1 in aqueous media to 100 nm PEGylated and DOX (doxorubicin)-rich micelles from which quantitative drug release is triggered by light; ( c ) Light directed DOX release, cell uptake, and cell death.

    Article Snippet: Materials and Instruments Doxorubicin hydrochloride (DOX·HCl) was purchased from Cayman Chemical Company (Ann Arbor, MI, USA) and used without further purification.

    Techniques: Construct

    Blocking Src's metabolic effect sensitizes cancer cells to pro-oxidant chemotherapy A, B. Src inhibitors and chemodrug Doxorubicin (Dox) show additive/synergistic effects on ROS induction and suppression of cell growth/viability. 4T1 cells were treated with Dox (1 μg/ml) and Src inhibitors SA and SU (1 μM each). ROS levels (A) and cell growth and viability (B) were subsequently determined. C, D. Expression of PDHA1 Y289F sensitizes cells to pro-oxidant. 4T1 cells transduced with WT or Y289F PDHA1 were treated with vehicle (DMSO) or Dox, followed by measurement of ROS levels (C) and cell growth and survival (D). Error bars represent S.D. *p

    Journal: Oncotarget

    Article Title: Src drives the Warburg effect and therapy resistance by inactivating pyruvate dehydrogenase through tyrosine-289 phosphorylation

    doi: 10.18632/oncotarget.7159

    Figure Lengend Snippet: Blocking Src's metabolic effect sensitizes cancer cells to pro-oxidant chemotherapy A, B. Src inhibitors and chemodrug Doxorubicin (Dox) show additive/synergistic effects on ROS induction and suppression of cell growth/viability. 4T1 cells were treated with Dox (1 μg/ml) and Src inhibitors SA and SU (1 μM each). ROS levels (A) and cell growth and viability (B) were subsequently determined. C, D. Expression of PDHA1 Y289F sensitizes cells to pro-oxidant. 4T1 cells transduced with WT or Y289F PDHA1 were treated with vehicle (DMSO) or Dox, followed by measurement of ROS levels (C) and cell growth and survival (D). Error bars represent S.D. *p

    Article Snippet: Src inhibitors PP2, SU6656 and Saracatinib were purchased from Cayman Chemical, and chemodrug Doxorubicin from Sigma.

    Techniques: Blocking Assay, Expressing, Transduction

    Pharmacological or genetic inhibition of DNM1L blocks mitochondrial fission and apoptosis induced by liensinine in combination with doxorubicin. ( A ) MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: Pharmacological or genetic inhibition of DNM1L blocks mitochondrial fission and apoptosis induced by liensinine in combination with doxorubicin. ( A ) MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Polyacrylamide Gel Electrophoresis, Inhibition, Multiple Displacement Amplification

    The combination of liensinine and doxorubicin inhibits tumor growth in a MDA-MB-231 mouse xenograft model. ( A ) Average tumor volume in vehicle control mice, mice treated with Lien (60 mg/kg) or Dox (2 mg/kg) or a combination of Lien and

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: The combination of liensinine and doxorubicin inhibits tumor growth in a MDA-MB-231 mouse xenograft model. ( A ) Average tumor volume in vehicle control mice, mice treated with Lien (60 mg/kg) or Dox (2 mg/kg) or a combination of Lien and

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Multiple Displacement Amplification, Mouse Assay

    Excessive accumulation of autophagosomes/mitophagosomes mediated by combination of liensinine and doxorubicin in MDA-MB-231 cells. ( A ) Cells were treated with vehicle, Lien (20 μM), Dox (0.2 μM) alone or combined treated

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: Excessive accumulation of autophagosomes/mitophagosomes mediated by combination of liensinine and doxorubicin in MDA-MB-231 cells. ( A ) Cells were treated with vehicle, Lien (20 μM), Dox (0.2 μM) alone or combined treated

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Multiple Displacement Amplification

    Autophagic inhibition combined with doxorubicin induces mitochondrial fission via dephosphorylation and mitochondrial translocation of DNM1L. ( A and D ) MDA-MB-231 cells were treated with vehicle, Lien (20 μM), Dox (0.2 μM)

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: Autophagic inhibition combined with doxorubicin induces mitochondrial fission via dephosphorylation and mitochondrial translocation of DNM1L. ( A and D ) MDA-MB-231 cells were treated with vehicle, Lien (20 μM), Dox (0.2 μM)

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Inhibition, De-Phosphorylation Assay, Translocation Assay, Multiple Displacement Amplification

    Liensinine sensitizes to a variety of anticancer drug-induced cell death in MDA-MB-231 and MCF-7 cells. ( A ) MDA-MB-231 and MCF-7 cells were treated with various concentrations of doxorubicin (Dox), paclitaxel, vincristine, cisplatin (CDDP), and staurosporine

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: Liensinine sensitizes to a variety of anticancer drug-induced cell death in MDA-MB-231 and MCF-7 cells. ( A ) MDA-MB-231 and MCF-7 cells were treated with various concentrations of doxorubicin (Dox), paclitaxel, vincristine, cisplatin (CDDP), and staurosporine

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Multiple Displacement Amplification

    Autophagosome/mitophagosome accumulation contributed to the combination effect of liensinine and doxorubicin. MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence of 3-MA (5 mM)

    Journal: Autophagy

    Article Title: A novel autophagy/mitophagy inhibitor liensinine sensitizes breast cancer cells to chemotherapy through DNM1L-mediated mitochondrial fission

    doi: 10.1080/15548627.2015.1056970

    Figure Lengend Snippet: Autophagosome/mitophagosome accumulation contributed to the combination effect of liensinine and doxorubicin. MDA-MB-231 cells were co-exposed to Lien (20 μM) and Dox (0.2 μM) in the presence or absence of 3-MA (5 mM)

    Article Snippet: Liensinine (2586–96–1) was purchased from MUST bio-technology, 3-methyladenine (M9281), rapamycin (R117), acridine orange (158550), chloroquine diphosphate salt (C6628), Thiazolyl Blue Tetrazolium Blue (MTT, M2128), paclitaxel (T7191), vincristine (V8879) and cisplatin (P4394) were purchased from Sigma-Aldrich, bafilomycin A1 (11038) was purchased from Cayman Chemical, doxorubicin (sc-200923) and staurosporine (sc-360258) were purchased from Santa Cruz Biotechnology, and Mdivi-1 (s7162) was from Selleck Chemicals.

    Techniques: Polyacrylamide Gel Electrophoresis, Multiple Displacement Amplification

    SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression regulated GSTP1/JNK signaling pathway A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Infection, Planar Chromatography, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunoprecipitation

    SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression sensitized HCC cells to chemotherapeutic agents A. Western blotting analysis of SIRT3 proteins in cells infected with lentivirus expressing SIRT3 or vector. GAPDH was used as a loading control. B-D. Cell viability of SIRT3-overexpressing cells exposed to chemotherapeutic agents. Forty-eight hour after lentivirus infection, SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) were treated with various concentrations of doxorubicin, cisplatin or epirubicin for 48 h. Cell viability was determined by MTS assay.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Western Blot, Infection, Expressing, Plasmid Preparation, Planar Chromatography, MTS Assay

    SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: SIRT3 overexpression enhanced chemotherapeutic agents-induced apoptosis in HCC cells A-C. Apoptosis in different groups was analyzed by flow cytometry with Annexin V/PI. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h and subjected to flow cytometry analysis. *, P

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Flow Cytometry, Cytometry, Infection, Planar Chromatography

    GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: GSTP1 overexpression or JNK inhibitor attenuate the sensitizing effect of SIRT3 A-B. GSTP1 overexpression abolished SIRT3-induced apoptosis in HCC cells treated with chemotherapeutic agents. SMMC-7721 and Huh-7 cells stably expressing SIRT3 were transfected with plasmid expressing GSTP1 and were then exposed to doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. Apoptotic ratio in different groups was detected by flow cytometry with Annexin V/PI(A) and PARP cleavage analysis (B). *, p

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Over Expression, Stable Transfection, Expressing, Transfection, Plasmid Preparation, Flow Cytometry, Cytometry

    Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.

    Journal: Oncotarget

    Article Title: Sirtuin 3 enhanced drug sensitivity of human hepatoma cells through glutathione S-transferase pi 1/JNK signaling pathway

    doi: 10.18632/oncotarget.10319

    Figure Lengend Snippet: Chemotherapeutic agents inhibited SIRT3 expression in HCC cells A. SIRT3 expression in three HCC cell lines (SMMC-7721, Huh-7 and PLC/PRF/5) and one immortalized liver cell line (MIHA) by using qPCR and western blotting analysis. β-actin mRNA expression was used as an internal control for qPCR. GAPDH was used as a loading control in western blotting analysis. B-D. Chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) inhibited SIRT3 expression. SMMC-7721(B), Huh-7(C) and PLC/PRF/5 (D) cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h before subjected to qPCR and western blotting analysis. E-F. The expression of SIRT3 was examined in SMMC-7721 and Huh-7 cells treated with various concentrations of chemotherapeutic agents (doxorubicin, cisplatin and epirubicin) by using western blotting analysis. GAPDH was used as a loading control.

    Article Snippet: Doxorubicin (D1515) and cisplatin (P4394) were obtained from Sigma-Aldrich (USA), epirubicin (56390-09-1) was obtained from Cayman Chemical (USA), Sorafenib (S7397) was obtained from Selleckchem (USA).

    Techniques: Expressing, Planar Chromatography, Real-time Polymerase Chain Reaction, Western Blot