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    ATCC a549 cells
    Abilities of different A. baumannii strains to cause cell death of <t>A549</t> alveolar cells. (A) Fluorescence microscopy images of human alveolar A549 cells infected with each of the A. baumannii strains and stained with the LIVE/DEAD Cellstain double-staining kit. Healthy cells with intact membranes are stained green, and dead cells with permeabilized membranes are stained red. A549 cells were incubated with the A. baumannii strains ATCC 19606 WT, AL1851 Δ lpxA , Al1852 Δ lpxD , AL1842 Δ lpxC , and ATCC 19606 pmrB for 20 h or left uninfected. (B) Quantification of A549 cell death caused by A. baumannii ATCC 19606 WT and AL1851 Δ lpxA , AL1852 Δ lpxD , and AL1842 Δ lpxC mutants and the pmrB mutant. The results of 6 independent experiments are shown as means and SD. *, P
    A549 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 9924 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore a549 cells
    Influence of recombinant NanA and NanB on expression of SA on the surface of <t>A549</t> cells . Cells were treated with different neuraminidase dilutions for 48 h. The lectins MAA (A) and SNA (B) were used to detect SAα2-3Gal and SAα2-6Gal, respectively, by immunocytochemical staining. Control (Co) was stained without using lectins.
    A549 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 3802 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Thermo Fisher a549 cells
    MTT assays. <t>A549</t> cells were treated with increasing concentration of XAV939 (0.1, 0.5, 1,5 and 10 µM) for 24, 4, 72 and 96 h. The result was shown as relative cell viability per concentration at each time point.
    A549 Cells, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 13422 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Becton Dickinson a549 cells
    Effects of trichostatin A (TSA) alone or in combination with quercetin on the growth (A) and apoptosis (B) of <t>A549</t> cells and H1299 cells. The cells were incubated with TSA (25 ng/mL) alone or in combination with 2 or 5 µM quercetin (2Q and 5Q, respectively) for 24 h and 48 h. Values (means ± SD, n = 3) at the same time not sharing a common letter (a-c and A-C for 24 and 48 h, respectively) are significantly different ( p
    A549 Cells, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 94/100, based on 1558 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Corning Life Sciences a549 cells
    Young’s modulus values expressed in kPa, calculated from the nuclear region and the cytoskeletal area of Caco-2 ( a ) and <t>A549</t> ( b ) cell lines after a treatment to 45 μg/ml of SiO 2 NPs and TiO 2 NPs for 72 h
    A549 Cells, supplied by Corning Life Sciences, used in various techniques. Bioz Stars score: 93/100, based on 809 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ribobio a549 cells
    Radiosensitizing effects of miR‐18a‐5p in vivo under irradiation. A, Growth curves of <t>A549</t> xenografts at day 10 (n = 6, P
    A549 Cells, supplied by Ribobio, used in various techniques. Bioz Stars score: 92/100, based on 181 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Abilities of different A. baumannii strains to cause cell death of A549 alveolar cells. (A) Fluorescence microscopy images of human alveolar A549 cells infected with each of the A. baumannii strains and stained with the LIVE/DEAD Cellstain double-staining kit. Healthy cells with intact membranes are stained green, and dead cells with permeabilized membranes are stained red. A549 cells were incubated with the A. baumannii strains ATCC 19606 WT, AL1851 Δ lpxA , Al1852 Δ lpxD , AL1842 Δ lpxC , and ATCC 19606 pmrB for 20 h or left uninfected. (B) Quantification of A549 cell death caused by A. baumannii ATCC 19606 WT and AL1851 Δ lpxA , AL1852 Δ lpxD , and AL1842 Δ lpxC mutants and the pmrB mutant. The results of 6 independent experiments are shown as means and SD. *, P

    Journal: Antimicrobial Agents and Chemotherapy

    Article Title: Biological Cost of Different Mechanisms of Colistin Resistance and Their Impact on Virulence in Acinetobacter baumannii

    doi: 10.1128/AAC.01597-13

    Figure Lengend Snippet: Abilities of different A. baumannii strains to cause cell death of A549 alveolar cells. (A) Fluorescence microscopy images of human alveolar A549 cells infected with each of the A. baumannii strains and stained with the LIVE/DEAD Cellstain double-staining kit. Healthy cells with intact membranes are stained green, and dead cells with permeabilized membranes are stained red. A549 cells were incubated with the A. baumannii strains ATCC 19606 WT, AL1851 Δ lpxA , Al1852 Δ lpxD , AL1842 Δ lpxC , and ATCC 19606 pmrB for 20 h or left uninfected. (B) Quantification of A549 cell death caused by A. baumannii ATCC 19606 WT and AL1851 Δ lpxA , AL1852 Δ lpxD , and AL1842 Δ lpxC mutants and the pmrB mutant. The results of 6 independent experiments are shown as means and SD. *, P

    Article Snippet: Infection of A549 cells with ATCC 19606 or the pmrB mutant resulted in greater loss of viability than with lpx mutants.

    Techniques: Fluorescence, Microscopy, Infection, Staining, Double Staining, Incubation, Mutagenesis

    Growth inhibitory effects of acetone extracts of Parmelia arseneana and Acarospora fuscata and isolated gyrophoric acid on FemX, A549, LS174 and K562 cell lines

    Journal: EXCLI Journal

    Article Title: Biological activities and chemical composition of lichens from Serbia

    doi:

    Figure Lengend Snippet: Growth inhibitory effects of acetone extracts of Parmelia arseneana and Acarospora fuscata and isolated gyrophoric acid on FemX, A549, LS174 and K562 cell lines

    Article Snippet: Cell culture Human colon carcinoma LS174 cells, human lung carcinoma A549 cells, malignant melanoma Fem-x cells and chronic myelogeneous leukaemia K562 cells (American Type Culture Collection, USA) were cultured as a monolayer in the RPMI 1640 nutrient medium, with 10 % (inactivated at 56 °C) FBS, 3 mM of L-glutamine, and antibiotics, at 37 °C in humidified air atmosphere with 5 % CO2 .

    Techniques: Isolation

    Prdx6 levels are sensitive to oxidative stress. ( A ) Primary cultures of human CEnCs) were treated with tert-butyl hydroperoxide (tBHP) for 3 h. pCEnCs were biotinylated and cell surface proteins purified by immunoprecipitation. The flow-through, unbound fraction served as a control for membrane fractionation. ( B ) pCEnCs and ( C ) A549 cells were treated with tBHP for 3 h and plasma membrane was isolated by density dependent centrifugation. Data from three independent experiments ± SEM is shown. Prdx6 levels were normalized to Na + /K + -ATPase and expressed relative to untreated (−) controls. Student t -test was performed to evaluate statistical significance (** p -value

    Journal: Antioxidants

    Article Title: Regulation of Oxidative Stress in Corneal Endothelial Cells by Prdx6

    doi: 10.3390/antiox7120180

    Figure Lengend Snippet: Prdx6 levels are sensitive to oxidative stress. ( A ) Primary cultures of human CEnCs) were treated with tert-butyl hydroperoxide (tBHP) for 3 h. pCEnCs were biotinylated and cell surface proteins purified by immunoprecipitation. The flow-through, unbound fraction served as a control for membrane fractionation. ( B ) pCEnCs and ( C ) A549 cells were treated with tBHP for 3 h and plasma membrane was isolated by density dependent centrifugation. Data from three independent experiments ± SEM is shown. Prdx6 levels were normalized to Na + /K + -ATPase and expressed relative to untreated (−) controls. Student t -test was performed to evaluate statistical significance (** p -value

    Article Snippet: The SV40-transformed human corneal endothelial cell line (B4G12, [ ]), the human lung adenocarcinoma A549 cell line (ATCC; CCL-185), HEK293T, and the spontaneous arising retinal pigmented epithelial cell line ARPE19 were maintained at 37 °C, 5% CO2 in DMEM (high glucose) supplemented with 10% bovine serum (Gibco; Thermo Fisher Scientific, Waltham, MA, USA) together with antibiotics.

    Techniques: Purification, Immunoprecipitation, Flow Cytometry, Fractionation, Isolation, Centrifugation

    CF mediated by FUT8 regulates the cancer-promoting capacity of CAFs via the modification of EGFR fucosylation. A. The expression of EGFR, p-EGFR, and FUT8 in primary CAFs and paired NLFs were tested by western blot analysis. C: CAFs. N: NLFs. B. The binding of fucose to EGFR was tested by immunoprecipitation (IP) and a lectin blot. C. Four shRNA fragments were used for the knockdown of FUT8 in CAFs, and the effect was tested by western blotting. D. A549 and H322 cells were cultured with CM from CAFs. The proliferation of NSCLC cells was tested by a clone formation assay. E. A549 and H322 cells were cultured with CM from CAFs/HLFs. The proliferation of NSCLC cells was tested by a clone formation assay. F, G. EGFR signaling and the phosphorylation levels of ERK, JAK, and Akt in CAFs or HLFs were tested by western blotting. NSC 228155 is an activator of EGFR that binds to the extracellular region of EGFR and enhances tyrosine phosphorylation of EGFR. Protein bands with the same subscript letter were transferred from the same SDS-PAGE gel. All experiments were repeated three times.

    Journal: American Journal of Cancer Research

    Article Title: α1,6-Fucosyltransferase (FUT8) regulates the cancer-promoting capacity of cancer-associated fibroblasts (CAFs) by modifying EGFR core fucosylation (CF) in non-small cell lung cancer (NSCLC)

    doi:

    Figure Lengend Snippet: CF mediated by FUT8 regulates the cancer-promoting capacity of CAFs via the modification of EGFR fucosylation. A. The expression of EGFR, p-EGFR, and FUT8 in primary CAFs and paired NLFs were tested by western blot analysis. C: CAFs. N: NLFs. B. The binding of fucose to EGFR was tested by immunoprecipitation (IP) and a lectin blot. C. Four shRNA fragments were used for the knockdown of FUT8 in CAFs, and the effect was tested by western blotting. D. A549 and H322 cells were cultured with CM from CAFs. The proliferation of NSCLC cells was tested by a clone formation assay. E. A549 and H322 cells were cultured with CM from CAFs/HLFs. The proliferation of NSCLC cells was tested by a clone formation assay. F, G. EGFR signaling and the phosphorylation levels of ERK, JAK, and Akt in CAFs or HLFs were tested by western blotting. NSC 228155 is an activator of EGFR that binds to the extracellular region of EGFR and enhances tyrosine phosphorylation of EGFR. Protein bands with the same subscript letter were transferred from the same SDS-PAGE gel. All experiments were repeated three times.

    Article Snippet: The human NSCLC cell lines A549 and H322 were obtained from The American Type Culture Collection (ATCC, Virginia, US).

    Techniques: Modification, Expressing, Western Blot, Binding Assay, Immunoprecipitation, shRNA, Cell Culture, Tube Formation Assay, SDS Page

    FUT8-mediated CF is necessary for the cancer-promoting capacity of CAFs. A. A lentivirus-packed FUT8 coding sequence was used to stably up-regulate FUT8 in HLFs. B. The effect of FUT8 up-regulation was tested by western blotting and lectin blotting analyses. C. The proliferation of A549 and H322 cells cultured with CM from CAFs or HLFs was tested by clone formation assays. D, E. A549 and H322 cells were co-cultured with fibroblasts in Transwell chambers, and the cell migration and invasion of NSCLC cells were tested. Magnification: 200×. F. Schematic diagram of the device used for the establishment of an in vitro non-contact co-culture system. A more detailed blueprint for 3D printing is available free from the corresponding authors upon request. 1: lid. 2: NSCLC cells. 3: CAFs/NLFs/HLFs. 4: precipitation well. G. The cell cycle of A549 and H322 cells co-cultured with fibroblasts was tested by PI staining and flow cytometry. Yellow peaks: diploids were observed in the assessed cells. H-J. A549 cells were co-cultured with fibroblasts in the non-contact co-culture system. The MAPK/ERK1/2 signaling pathway and biomarkers of EMT and the G1/S checkpoint in A549 cells were tested by western blot analysis. Protein bands with the same subscript letter were transferred from the same SDS-PAGE gel. All experiments were repeated three times.

    Journal: American Journal of Cancer Research

    Article Title: α1,6-Fucosyltransferase (FUT8) regulates the cancer-promoting capacity of cancer-associated fibroblasts (CAFs) by modifying EGFR core fucosylation (CF) in non-small cell lung cancer (NSCLC)

    doi:

    Figure Lengend Snippet: FUT8-mediated CF is necessary for the cancer-promoting capacity of CAFs. A. A lentivirus-packed FUT8 coding sequence was used to stably up-regulate FUT8 in HLFs. B. The effect of FUT8 up-regulation was tested by western blotting and lectin blotting analyses. C. The proliferation of A549 and H322 cells cultured with CM from CAFs or HLFs was tested by clone formation assays. D, E. A549 and H322 cells were co-cultured with fibroblasts in Transwell chambers, and the cell migration and invasion of NSCLC cells were tested. Magnification: 200×. F. Schematic diagram of the device used for the establishment of an in vitro non-contact co-culture system. A more detailed blueprint for 3D printing is available free from the corresponding authors upon request. 1: lid. 2: NSCLC cells. 3: CAFs/NLFs/HLFs. 4: precipitation well. G. The cell cycle of A549 and H322 cells co-cultured with fibroblasts was tested by PI staining and flow cytometry. Yellow peaks: diploids were observed in the assessed cells. H-J. A549 cells were co-cultured with fibroblasts in the non-contact co-culture system. The MAPK/ERK1/2 signaling pathway and biomarkers of EMT and the G1/S checkpoint in A549 cells were tested by western blot analysis. Protein bands with the same subscript letter were transferred from the same SDS-PAGE gel. All experiments were repeated three times.

    Article Snippet: The human NSCLC cell lines A549 and H322 were obtained from The American Type Culture Collection (ATCC, Virginia, US).

    Techniques: Sequencing, Stable Transfection, Western Blot, Cell Culture, Migration, In Vitro, Co-Culture Assay, Staining, Flow Cytometry, SDS Page

    (A) The catalytic antioxidant MnTDE-1,3-IP 5+ (MnP, 5 μM) protected A549 cells against Cas IIgly-induced injury (7.5 μM, 24 h treatment). (B) H157 cells required higher amounts of MnTDE-1,3-IP 5+ (MnP, 20 μM) to protect against Cas

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: (A) The catalytic antioxidant MnTDE-1,3-IP 5+ (MnP, 5 μM) protected A549 cells against Cas IIgly-induced injury (7.5 μM, 24 h treatment). (B) H157 cells required higher amounts of MnTDE-1,3-IP 5+ (MnP, 20 μM) to protect against Cas

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques:

    (A) Cas IIgly (5 μM, 6 h) induced mitochondrial DNA (mtDNA) damage in A549 cells, as detected by amplification efficiency assay. Bars with different letters are statistically different from one another ( n = 3, P

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: (A) Cas IIgly (5 μM, 6 h) induced mitochondrial DNA (mtDNA) damage in A549 cells, as detected by amplification efficiency assay. Bars with different letters are statistically different from one another ( n = 3, P

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques: Amplification

    Cas IIgly (2.5 μM, 6 h) induced the expression of heme oxygenase-1 (HO-1, 35 Kd) in H157 and A547 cells, as shown by immunoblotting. GAPDH (40 Kd) was used as loading control. It is worth noting that A549 but not H157 cells showed basal levels

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: Cas IIgly (2.5 μM, 6 h) induced the expression of heme oxygenase-1 (HO-1, 35 Kd) in H157 and A547 cells, as shown by immunoblotting. GAPDH (40 Kd) was used as loading control. It is worth noting that A549 but not H157 cells showed basal levels

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques: Expressing

    (A) Cas IIgly (6 h treatment) produced a dramatic loss ( > 70%) in intracellular glutathione (GSH) levels in A549 and H157 cells using 5 μM and 2.5 μM Cas IIgly, respectively, compared to control (Co). The 100% values for both cell

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: (A) Cas IIgly (6 h treatment) produced a dramatic loss ( > 70%) in intracellular glutathione (GSH) levels in A549 and H157 cells using 5 μM and 2.5 μM Cas IIgly, respectively, compared to control (Co). The 100% values for both cell

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques: Produced

    (A) As shown in A549 cells, most of the intracellular GSH loss accounted as its oxidized disulfide form GSSG; following treatment of the lysate with glutathione reductase (GR), 63% of the GSH loss was recovered. Bars with different letters are statistically

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: (A) As shown in A549 cells, most of the intracellular GSH loss accounted as its oxidized disulfide form GSSG; following treatment of the lysate with glutathione reductase (GR), 63% of the GSH loss was recovered. Bars with different letters are statistically

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques:

    (A and B) A549 cells treated with Cas IIgly (5 μM, 12 and 24 h) showed increased levels of ROS, as shown by flow cytometry using MitoSOX fluorescence (FL2 channel). (C and E) A549 cells also showed a loss of Rho123 fluorescence (FL1 channel) and

    Journal:

    Article Title: Casiope?na IIgly-induced oxidative stress and mitochondrial dysfunction in human lung cancer A549 and H157 cells

    doi: 10.1016/j.tox.2009.12.010

    Figure Lengend Snippet: (A and B) A549 cells treated with Cas IIgly (5 μM, 12 and 24 h) showed increased levels of ROS, as shown by flow cytometry using MitoSOX fluorescence (FL2 channel). (C and E) A549 cells also showed a loss of Rho123 fluorescence (FL1 channel) and

    Article Snippet: Human lung cancer A549 cells were purchased from ATCC (Manassas, VA) were grown in Ham’s F-12 medium with 2 mM L-glutamine (ATCC) supplemented with 10% fetal bovine serum (FBS) and 1% pen/strep (10,000 unit, Cellgro), as commonly used for this cell line, at 37°C and 5% CO2 air atmosphere.

    Techniques: Flow Cytometry, Cytometry, Fluorescence

    ZM447439 inhibits Aurora A and Aurora B. (A) Chemical structure of ZM447439. (B) Table showing the IC 50 values (μM) of ZM447439 against a panel of protein kinases. (C) DNA content histograms of HeLa, A549, and HME cells treated with ZM447439 for the times indicated in hours. (D) Mitotic DLD-1 cells stained for phosphohistone H3 (green) and DNA (red).

    Journal: The Journal of Cell Biology

    Article Title: Aurora B couples chromosome alignment with anaphase by targeting BubR1, Mad2, and Cenp-E to kinetochores

    doi: 10.1083/jcb.200208091

    Figure Lengend Snippet: ZM447439 inhibits Aurora A and Aurora B. (A) Chemical structure of ZM447439. (B) Table showing the IC 50 values (μM) of ZM447439 against a panel of protein kinases. (C) DNA content histograms of HeLa, A549, and HME cells treated with ZM447439 for the times indicated in hours. (D) Mitotic DLD-1 cells stained for phosphohistone H3 (green) and DNA (red).

    Article Snippet: Cell culture A549, MCF-7, and DLD-1 cells (American Type Culture Collection), TA-HeLa cells , U2OS cells stably transfected with pCMVp53 143A, and parental U2OS cells (both from Karen Vousden, Beatson Institute for Cancer Research, Glasgow, UK) were all cultured as described previously ( ).

    Techniques: Staining

    Positional profiles of phenotypic consequences of individual nucleotides at individual siRNA positions. ( A – C ). (A, B) Positional profile for cell count and infection phenotypes, respectively, in a genome-wide Brucella abortus screen in HeLa CCL2 cells conducted with a non-pooled siRNA library (Qiagen). (C) siRNA nucleotide positional profile for cell count in a genome-wide screen for Salmonella entry into MEFs (murine embryonic fibroblasts, unpublished). ( D ) Global comparison of siRNA nucleotide profiles, generated for three different pathogen screens ( Brucella abortus, Salmonella Typhimurium and Adenovirus ), across three different libraries of non-pooled siRNAs designed by Qiagen, Dharmacon and Ambion (QU, DU and AU, respectively) targeting human kinome genes (∼ 800) in HeLa CCL2 cells, together with another genome-wide screen carried out in human A549 cells and mouse embryonic fibroblast cells using non-pooled Dharmacon (DU) and Qiagen libraries (QUM), respectively. Each data point represents the entire nucleotide profile as seen in panels A–C. Black color denotes cell count readouts and gray color denotes infection readouts.

    Journal: Nucleic Acids Research

    Article Title: Growth-restricting effects of siRNA transfections: a largely deterministic combination of off-target binding and hybridization-independent competition

    doi: 10.1093/nar/gky798

    Figure Lengend Snippet: Positional profiles of phenotypic consequences of individual nucleotides at individual siRNA positions. ( A – C ). (A, B) Positional profile for cell count and infection phenotypes, respectively, in a genome-wide Brucella abortus screen in HeLa CCL2 cells conducted with a non-pooled siRNA library (Qiagen). (C) siRNA nucleotide positional profile for cell count in a genome-wide screen for Salmonella entry into MEFs (murine embryonic fibroblasts, unpublished). ( D ) Global comparison of siRNA nucleotide profiles, generated for three different pathogen screens ( Brucella abortus, Salmonella Typhimurium and Adenovirus ), across three different libraries of non-pooled siRNAs designed by Qiagen, Dharmacon and Ambion (QU, DU and AU, respectively) targeting human kinome genes (∼ 800) in HeLa CCL2 cells, together with another genome-wide screen carried out in human A549 cells and mouse embryonic fibroblast cells using non-pooled Dharmacon (DU) and Qiagen libraries (QUM), respectively. Each data point represents the entire nucleotide profile as seen in panels A–C. Black color denotes cell count readouts and gray color denotes infection readouts.

    Article Snippet: Secondly, despite being trained on HeLa CCL2 cells only, the model was able to predict cell counts not only in HeLa cells (with up to 70% accuracy, Figure ) but also in A549 (cancerous cells; adenocarcinomic human alveolar basal epithelial cells) and WI38 (normal diploid fibroblasts derived from lung tissue) cells to about 60% and 50% accuracy, respectively (Figure ).

    Techniques: Cell Counting, Infection, Genome Wide, Generated

    The lactate dehydrogenase (LDH)release of A549 cells by co-incubating with S. aureus and various concentrations of coptisine. The data were present as mean ± SD ( n = 3). * indicates p

    Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

    Article Title: Novel Inhibitor Discovery of Staphylococcus aureus Sortase B and the Mechanism Confirmation via Molecular Modeling

    doi: 10.3390/molecules23040977

    Figure Lengend Snippet: The lactate dehydrogenase (LDH)release of A549 cells by co-incubating with S. aureus and various concentrations of coptisine. The data were present as mean ± SD ( n = 3). * indicates p

    Article Snippet: Adhesion Assay Mediated by S. aureus According to a method reported previously [ ] with some modifications, human lung epithelial A549 cells (ATCC) were cultured with complete DMEM medium (DMEM with 10% fetal bovine serum and 100IU/mL of penicillin and streptomycin).

    Techniques:

    Cathepsin B plays an important role in lung cancer cell migration. a , The effect of the cathepsin B inhibitor CA-074Me on the EGF-stimulated lung cancer A549 cell migration determined by the wound healing assay. b , The effect of the cathepsin B inhibitor CA-074Me on the EGF-stimulated lung cancer A549 cell migration determined by the transwell assay. c , Quantification of the data from three independent transwell migration experiments. The statistics was performed with the treatment sample vs its control. ***, p

    Journal: Molecular Cancer

    Article Title: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells

    doi: 10.1186/s12943-018-0784-2

    Figure Lengend Snippet: Cathepsin B plays an important role in lung cancer cell migration. a , The effect of the cathepsin B inhibitor CA-074Me on the EGF-stimulated lung cancer A549 cell migration determined by the wound healing assay. b , The effect of the cathepsin B inhibitor CA-074Me on the EGF-stimulated lung cancer A549 cell migration determined by the transwell assay. c , Quantification of the data from three independent transwell migration experiments. The statistics was performed with the treatment sample vs its control. ***, p

    Article Snippet: The lung cancer cell lines A549 and H1650 were purchased from ATCC.

    Techniques: Migration, Wound Healing Assay, Transwell Assay

    NEDD4 mediates EGFR-dependent lung cancer cell migration. a , Wound healing assay of A549 cell migration. Left top panel, the knockdown of NEDD4 by shNEDD4 (lane 2) and recovery of NEDD4 upon re-introducing NEDD4 cDNA in the knockdown cells (lane 3); NEDD4-HM, high molecular weight NEDD4; NEDD4-LM, low molecular weight NEDD4. Left bottom panel, the protein level of EGFR in the lung cancer cell lines A549 and H1650 shown by immunoblotting with the cell lysates. Middle panel, photo images of the cell migration. Right panel, quantification of the EGF-stimulated cell migration area occupied after 24 h from the data of three independent experiments using the imaging software Image J (NIH). The non-EGF-treated cell migration area was subtracted by the EGF-treated cell migration area to obtain the EGF-stimulated cell migration area. b , Transwell assay of A549 cell migration. Note that the small lightly-stained round dots are pores of the transwell plates (sh NEDD4 panels). c , Wound healing assay of H1650 cells

    Journal: Molecular Cancer

    Article Title: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells

    doi: 10.1186/s12943-018-0784-2

    Figure Lengend Snippet: NEDD4 mediates EGFR-dependent lung cancer cell migration. a , Wound healing assay of A549 cell migration. Left top panel, the knockdown of NEDD4 by shNEDD4 (lane 2) and recovery of NEDD4 upon re-introducing NEDD4 cDNA in the knockdown cells (lane 3); NEDD4-HM, high molecular weight NEDD4; NEDD4-LM, low molecular weight NEDD4. Left bottom panel, the protein level of EGFR in the lung cancer cell lines A549 and H1650 shown by immunoblotting with the cell lysates. Middle panel, photo images of the cell migration. Right panel, quantification of the EGF-stimulated cell migration area occupied after 24 h from the data of three independent experiments using the imaging software Image J (NIH). The non-EGF-treated cell migration area was subtracted by the EGF-treated cell migration area to obtain the EGF-stimulated cell migration area. b , Transwell assay of A549 cell migration. Note that the small lightly-stained round dots are pores of the transwell plates (sh NEDD4 panels). c , Wound healing assay of H1650 cells

    Article Snippet: The lung cancer cell lines A549 and H1650 were purchased from ATCC.

    Techniques: Migration, Wound Healing Assay, Molecular Weight, Imaging, Software, Transwell Assay, Staining

    NEDD4 is associated with activated EGFR. a , Co-immunoprecipitation of NEDD4 with activated EGFR in lung cancer cells. Lung cancer A549 or H358 cells were serum-starved for 12 h followed by stimulation with EGF (50 ng/ml) for indicated times. EGFR was immunoprecipitated with anti-EGFR (Mab528) and detected by immunoblotting with anti-EGFR (1005) (top panels). Co-immunoprecipitated NEDD4 was detected by immunoblotting with an anti-NEDD4 (second top panels). The level of EGFR and NEDD4 in the cell lysates was also detected by immunoblotting (middle and second bottom panels). Notice that EGFR in A549 and H358 cells has an EGF-induced degradation. b , Internalized EGFR is co-localized with NEDD4. A549 cells were serum-starved for 12 h followed by stimulation with EGF (50 ng/ml) for 0 or 60 min. The cells were immuno-stained with anti-EGFR (1005) (red) and anti-NEDD4 (green). Bar, 20 μM. c , Co-expression of NEDD4 with EGFR in lung adenocarcinoma tissue. The tissue microarray containing 63 lung adenocarcinoma section samples was immunohistochemically stained with anti-EGFR or anti-NEDD4

    Journal: Molecular Cancer

    Article Title: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells

    doi: 10.1186/s12943-018-0784-2

    Figure Lengend Snippet: NEDD4 is associated with activated EGFR. a , Co-immunoprecipitation of NEDD4 with activated EGFR in lung cancer cells. Lung cancer A549 or H358 cells were serum-starved for 12 h followed by stimulation with EGF (50 ng/ml) for indicated times. EGFR was immunoprecipitated with anti-EGFR (Mab528) and detected by immunoblotting with anti-EGFR (1005) (top panels). Co-immunoprecipitated NEDD4 was detected by immunoblotting with an anti-NEDD4 (second top panels). The level of EGFR and NEDD4 in the cell lysates was also detected by immunoblotting (middle and second bottom panels). Notice that EGFR in A549 and H358 cells has an EGF-induced degradation. b , Internalized EGFR is co-localized with NEDD4. A549 cells were serum-starved for 12 h followed by stimulation with EGF (50 ng/ml) for 0 or 60 min. The cells were immuno-stained with anti-EGFR (1005) (red) and anti-NEDD4 (green). Bar, 20 μM. c , Co-expression of NEDD4 with EGFR in lung adenocarcinoma tissue. The tissue microarray containing 63 lung adenocarcinoma section samples was immunohistochemically stained with anti-EGFR or anti-NEDD4

    Article Snippet: The lung cancer cell lines A549 and H1650 were purchased from ATCC.

    Techniques: Immunoprecipitation, Staining, Expressing, Microarray

    NEDD4 is required for EGF-stimulated lysosomal secretion of cathepsin B. a , Lysosomes function in lung cancer cell migration. A549 cells were resuspended in serum-free medium and used for transwell cell migration assay. The migration attractant was 10% fetal bovine serum plus or minus EGF (50 ng/ml). The lysosome inhibitors chloroquine (10 μM) was added in the medium with EGF. The cells migrated from the top well to the bottom well within 6 h. The migrated cells were stained and quantified as described in the section of Methods. b , Overexpression of the NEDD4 ligase-dead mutant NEDD4[C867A] eliminated the LAMP2-positive vesicles at cell edges. NEDD4 or the ligase-dead mutant was stably expressed in A549 cells. The cells were stimulated with EGF (50 ng/ml) for 30 min, followed by immunofluorescent staining. NEDD4 and LAMP2 were stained with anti-NEDD4 and anti-LAMP2. The white arrows indicate the putative lysosomal secretion vesicles. NEDD4-LD stands for the ligase-dead mutant of NEDD4, NEDD4[C867A]. Bar, 20 μM. c , The culture medium collected from the vector control or shNEDD4 cells treated with or without EGF for 12 h was used for detection of cathepsin B with a human cathepsin B ELISA assay kit. The assay was repeated three times. ***, p

    Journal: Molecular Cancer

    Article Title: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells

    doi: 10.1186/s12943-018-0784-2

    Figure Lengend Snippet: NEDD4 is required for EGF-stimulated lysosomal secretion of cathepsin B. a , Lysosomes function in lung cancer cell migration. A549 cells were resuspended in serum-free medium and used for transwell cell migration assay. The migration attractant was 10% fetal bovine serum plus or minus EGF (50 ng/ml). The lysosome inhibitors chloroquine (10 μM) was added in the medium with EGF. The cells migrated from the top well to the bottom well within 6 h. The migrated cells were stained and quantified as described in the section of Methods. b , Overexpression of the NEDD4 ligase-dead mutant NEDD4[C867A] eliminated the LAMP2-positive vesicles at cell edges. NEDD4 or the ligase-dead mutant was stably expressed in A549 cells. The cells were stimulated with EGF (50 ng/ml) for 30 min, followed by immunofluorescent staining. NEDD4 and LAMP2 were stained with anti-NEDD4 and anti-LAMP2. The white arrows indicate the putative lysosomal secretion vesicles. NEDD4-LD stands for the ligase-dead mutant of NEDD4, NEDD4[C867A]. Bar, 20 μM. c , The culture medium collected from the vector control or shNEDD4 cells treated with or without EGF for 12 h was used for detection of cathepsin B with a human cathepsin B ELISA assay kit. The assay was repeated three times. ***, p

    Article Snippet: The lung cancer cell lines A549 and H1650 were purchased from ATCC.

    Techniques: Migration, Cell Migration Assay, Staining, Over Expression, Mutagenesis, Stable Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay

    NEDD4 does not ubiquitinate and downregulate PTEN. a , NEDD4 was co-expressed with flag-PTEN or Myc-ACK1 by transfection in HEK293 cells. Ubiquitinated ACK1 or PTEN was precipitated with bead-bound GST-Uba from the cell lysates followed by immunoblotting with anti-Myc or anti-flag antibodies. b , Lung cancer A549 cells were infected with lenti-viral vector pLKO.1 or the vector-loaded sh NEDD4 . NEDD4 in the cell lysates was detected by immunoblotting with anti-NEDD4 (second top panel). The effect of knockdown NEDD4 on expression of PTEN and activation of AKT was assessed by immunoblotting PTEN AKT or phospho-AKT in the cell lysates with their antibodies respectively. c , Immunohistochemical (IHC) staining of 63 human lung adenocarcinoma tumors with anti-NEDD4 and anti-PTEN antibodies. The positive tumor samples were assessed and counted under microscope and listed in the table

    Journal: Molecular Cancer

    Article Title: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells

    doi: 10.1186/s12943-018-0784-2

    Figure Lengend Snippet: NEDD4 does not ubiquitinate and downregulate PTEN. a , NEDD4 was co-expressed with flag-PTEN or Myc-ACK1 by transfection in HEK293 cells. Ubiquitinated ACK1 or PTEN was precipitated with bead-bound GST-Uba from the cell lysates followed by immunoblotting with anti-Myc or anti-flag antibodies. b , Lung cancer A549 cells were infected with lenti-viral vector pLKO.1 or the vector-loaded sh NEDD4 . NEDD4 in the cell lysates was detected by immunoblotting with anti-NEDD4 (second top panel). The effect of knockdown NEDD4 on expression of PTEN and activation of AKT was assessed by immunoblotting PTEN AKT or phospho-AKT in the cell lysates with their antibodies respectively. c , Immunohistochemical (IHC) staining of 63 human lung adenocarcinoma tumors with anti-NEDD4 and anti-PTEN antibodies. The positive tumor samples were assessed and counted under microscope and listed in the table

    Article Snippet: The lung cancer cell lines A549 and H1650 were purchased from ATCC.

    Techniques: Transfection, Infection, Plasmid Preparation, Expressing, Activation Assay, Immunohistochemistry, Staining, Microscopy

    Activity of the wild-type p5 and p19 promoters. (A) Diagram of the p5 and p19 promoter elements in the CAT reporter constructs p5CAT, pIM45CAT3, and psub262CAT3. The asterisk indicates a stop codon in the Rep78 open reading frame at amino acid position 71. (B to D) Graphic representation of CAT activity from the p5CAT, pIM45CAT3, and psub262CAT3 reporter constructs after transfection in A549 cells in the presence of plasmid alone (Mock) or with the addition of 1 μg of pIM45 (Rep), Ad at an MOI of 5 (Ad), or 1 μg of pIM45 and Ad at an MOI of 5 (Ad Rep). Error bars indicate 1 SD.

    Journal: Journal of Virology

    Article Title: Studies of the Mechanism of Transactivation of the Adeno-Associated Virus p19 Promoter by Rep Protein

    doi: 10.1128/JVI.76.16.8225-8235.2002

    Figure Lengend Snippet: Activity of the wild-type p5 and p19 promoters. (A) Diagram of the p5 and p19 promoter elements in the CAT reporter constructs p5CAT, pIM45CAT3, and psub262CAT3. The asterisk indicates a stop codon in the Rep78 open reading frame at amino acid position 71. (B to D) Graphic representation of CAT activity from the p5CAT, pIM45CAT3, and psub262CAT3 reporter constructs after transfection in A549 cells in the presence of plasmid alone (Mock) or with the addition of 1 μg of pIM45 (Rep), Ad at an MOI of 5 (Ad), or 1 μg of pIM45 and Ad at an MOI of 5 (Ad Rep). Error bars indicate 1 SD.

    Article Snippet: Human A549 cells (ATCC CCL 185) were maintained in Dulbecco's modified essential medium (DMEM; Gibco BRL) containing 10% bovine calf serum (HyClone Laboratories, Inc.) at 37°C in 100-mm-diameter culture dishes.

    Techniques: Activity Assay, Construct, Transfection, Plasmid Preparation

    Baseline-adjusted SB (A) and FPG sites (B) in A549 cell cultures exposed 24 hours to SRM1650, SRM2975 and ASPM. The data are obtained from figure 4 and table 1. Data points are mean ± SEM (SRMs, n = 9; ASPM, n = 6). There was no significant difference between the particle's ability to induce SB and FPG sites at any doses ( p > 0.05, Kruskal-Wallis test).

    Journal: Particle and Fibre Toxicology

    Article Title: DNA damage and cytotoxicity in type II lung epithelial (A549) cell cultures after exposure to diesel exhaust and urban street particles

    doi: 10.1186/1743-8977-5-6

    Figure Lengend Snippet: Baseline-adjusted SB (A) and FPG sites (B) in A549 cell cultures exposed 24 hours to SRM1650, SRM2975 and ASPM. The data are obtained from figure 4 and table 1. Data points are mean ± SEM (SRMs, n = 9; ASPM, n = 6). There was no significant difference between the particle's ability to induce SB and FPG sites at any doses ( p > 0.05, Kruskal-Wallis test).

    Article Snippet: Cell culture A549 cells (American Type Culture Collection, Manassas, VA, USA), kindly provided by the National Research Centre for the Working Environment, Denmark, were grown in F12 nutrient mixture (HAM) supplemented with 10% heat inactivated foetal bovine serum, 1% L-glutamine and 1% penicillin-streptomycin (incubation at 37°C, 5% CO2 ).

    Techniques:

    Cytotoxicity of A549 cells exposed to SRM2975 (solid bars), SRM1650 (hatched bars) and ASPM (open bars). The 100% maximum LDH release is obtained by treatment of cell cultures with Triton X-100, whereas the baseline LDH release in untreated cell cultures is 0%. Bars denote the mean ± SEM; (n = 3). * Statistically significant compared to control p

    Journal: Particle and Fibre Toxicology

    Article Title: DNA damage and cytotoxicity in type II lung epithelial (A549) cell cultures after exposure to diesel exhaust and urban street particles

    doi: 10.1186/1743-8977-5-6

    Figure Lengend Snippet: Cytotoxicity of A549 cells exposed to SRM2975 (solid bars), SRM1650 (hatched bars) and ASPM (open bars). The 100% maximum LDH release is obtained by treatment of cell cultures with Triton X-100, whereas the baseline LDH release in untreated cell cultures is 0%. Bars denote the mean ± SEM; (n = 3). * Statistically significant compared to control p

    Article Snippet: Cell culture A549 cells (American Type Culture Collection, Manassas, VA, USA), kindly provided by the National Research Centre for the Working Environment, Denmark, were grown in F12 nutrient mixture (HAM) supplemented with 10% heat inactivated foetal bovine serum, 1% L-glutamine and 1% penicillin-streptomycin (incubation at 37°C, 5% CO2 ).

    Techniques:

    DNA damage measured by the comet assay in A549 cells exposed to SRM2975 and SRM1650 for 3, 24 or 48 hours. (A) SB, SRM2975, (B) FPG sites, SRM2975, (C) SB, SRM1650 and (D) FPG sites, SRM1650. Mean ± SEM, n = 9. * Dose where all exposure times are statistically significant compared to control ( p

    Journal: Particle and Fibre Toxicology

    Article Title: DNA damage and cytotoxicity in type II lung epithelial (A549) cell cultures after exposure to diesel exhaust and urban street particles

    doi: 10.1186/1743-8977-5-6

    Figure Lengend Snippet: DNA damage measured by the comet assay in A549 cells exposed to SRM2975 and SRM1650 for 3, 24 or 48 hours. (A) SB, SRM2975, (B) FPG sites, SRM2975, (C) SB, SRM1650 and (D) FPG sites, SRM1650. Mean ± SEM, n = 9. * Dose where all exposure times are statistically significant compared to control ( p

    Article Snippet: Cell culture A549 cells (American Type Culture Collection, Manassas, VA, USA), kindly provided by the National Research Centre for the Working Environment, Denmark, were grown in F12 nutrient mixture (HAM) supplemented with 10% heat inactivated foetal bovine serum, 1% L-glutamine and 1% penicillin-streptomycin (incubation at 37°C, 5% CO2 ).

    Techniques: Single Cell Gel Electrophoresis

    Epo co-medication reduces tumor growth but increases the relative blood volume in carboplatin-treated NSCLC-xenografts. A : The tumor volumes, as measured by 3D ultrasound, were significantly lower in Epo co-medicated (Cp + Epo 5 and Cp + Epo 20) A549 (left) and H838 (right) compared with only carboplatin-treated (Cp) tumors starting from week one of therapy (*p

    Journal: Theranostics

    Article Title: Erythropoietin Improves the Accumulation and Therapeutic Effects of Carboplatin by Enhancing Tumor Vascularization and Perfusion

    doi: 10.7150/thno.11304

    Figure Lengend Snippet: Epo co-medication reduces tumor growth but increases the relative blood volume in carboplatin-treated NSCLC-xenografts. A : The tumor volumes, as measured by 3D ultrasound, were significantly lower in Epo co-medicated (Cp + Epo 5 and Cp + Epo 20) A549 (left) and H838 (right) compared with only carboplatin-treated (Cp) tumors starting from week one of therapy (*p

    Article Snippet: Cell lines and cell culture The NSCLC cell lines A549 and H838 (both ATCC) were cultivated in Dulbecco's Modified Eagle's Medium (DMEM), 1% penicillin-streptomycin, and 10% fetal calf serum (all Invitrogen).

    Techniques:

    In vitro cytotoxicity profile of blank CPNPs and Dtxls-en-CPNPs against A549 cells.

    Journal: Micromachines

    Article Title: A Method to Encapsulate Small Organic Molecules in Calcium Phosphate Nanoparticles Based on the Supramolecular Chemistry of Cyclodextrin

    doi: 10.3390/mi8100291

    Figure Lengend Snippet: In vitro cytotoxicity profile of blank CPNPs and Dtxls-en-CPNPs against A549 cells.

    Article Snippet: Cell Culture The human lung cancer cell line A549 (ATCC) (Shanghai Fumengjiyin Biotechnology Co., Ltd., Shanghai, China) were cultured in DMEM (Gibco, Carlsbad, CA, USA) with 10% fetal bovine serum (Gibco) at 37 °C with 5% CO2 humidified atmosphere.

    Techniques: In Vitro

    Confocal laser scanning microscopy observation of A549 cells incubated with RBs-en-CPNPs. The red fluorescence represented the intracellular RBs signal. Cell nuclei and the cytoskeleton were stained with DAPI (Blue) and Alexa Fluor 488 phalloidin (Green), respectively. Scale bar = 10 μm.

    Journal: Micromachines

    Article Title: A Method to Encapsulate Small Organic Molecules in Calcium Phosphate Nanoparticles Based on the Supramolecular Chemistry of Cyclodextrin

    doi: 10.3390/mi8100291

    Figure Lengend Snippet: Confocal laser scanning microscopy observation of A549 cells incubated with RBs-en-CPNPs. The red fluorescence represented the intracellular RBs signal. Cell nuclei and the cytoskeleton were stained with DAPI (Blue) and Alexa Fluor 488 phalloidin (Green), respectively. Scale bar = 10 μm.

    Article Snippet: Cell Culture The human lung cancer cell line A549 (ATCC) (Shanghai Fumengjiyin Biotechnology Co., Ltd., Shanghai, China) were cultured in DMEM (Gibco, Carlsbad, CA, USA) with 10% fetal bovine serum (Gibco) at 37 °C with 5% CO2 humidified atmosphere.

    Techniques: Confocal Laser Scanning Microscopy, Incubation, Fluorescence, Staining

    TTP destabilizes MEP1A mRNA. A , representative Western blot showing overexpression of TTP protein by pcDNA-hTTP in transiently transfected A549 cells compared with the loading control, β-actin. B , A549 cells were transiently cotransfected with

    Journal: The Journal of Biological Chemistry

    Article Title: Post-transcriptional Regulation of Meprin ? by the RNA-binding Proteins Hu Antigen R (HuR) and Tristetraprolin (TTP) *

    doi: 10.1074/jbc.M112.444208

    Figure Lengend Snippet: TTP destabilizes MEP1A mRNA. A , representative Western blot showing overexpression of TTP protein by pcDNA-hTTP in transiently transfected A549 cells compared with the loading control, β-actin. B , A549 cells were transiently cotransfected with

    Article Snippet: A549 human lung carcinoma cells (ATCC) were grown under similar conditions in F12K medium (ATCC) supplemented with 10% FBS, 100 units/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Western Blot, Over Expression, Transfection

    FOXD3-AS1 promoted chemo-resistance in NSCLC cells. a qRT-PCR determination of FOXD3-AS1 in cell lines including NHBE, A549, H1299, A549/DDP and H1299/DDP. b qRT-PCR determination of FOXD3-AS1 in A549 and H1299 cells with pcDNA3.1 or pcDNA3.1-FOXD3-AS1 transfection. c – e CCK-8 assay determination of IC50 values (cisplatin) in A549 and H1299 cells with pcDNA3.1 or pcDNA3.1-FOXD3-AS1 transfection. f qRT-PCR determination of FOXD3-AS1 in A549 and H1299 cells with si-NC or si-FOXD3-AS1 transfection. g – i CCK-8 assay determination of IC50 values (cisplatin) in A549 and H1299 cells with si-NC or si-FOXD3-AS1 transfection. N = 3 biological samples, and each sample was assayed in triplicates. Significant different between different treatment groups were shown as *P

    Journal: Cancer Cell International

    Article Title: LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis

    doi: 10.1186/s12935-020-01402-9

    Figure Lengend Snippet: FOXD3-AS1 promoted chemo-resistance in NSCLC cells. a qRT-PCR determination of FOXD3-AS1 in cell lines including NHBE, A549, H1299, A549/DDP and H1299/DDP. b qRT-PCR determination of FOXD3-AS1 in A549 and H1299 cells with pcDNA3.1 or pcDNA3.1-FOXD3-AS1 transfection. c – e CCK-8 assay determination of IC50 values (cisplatin) in A549 and H1299 cells with pcDNA3.1 or pcDNA3.1-FOXD3-AS1 transfection. f qRT-PCR determination of FOXD3-AS1 in A549 and H1299 cells with si-NC or si-FOXD3-AS1 transfection. g – i CCK-8 assay determination of IC50 values (cisplatin) in A549 and H1299 cells with si-NC or si-FOXD3-AS1 transfection. N = 3 biological samples, and each sample was assayed in triplicates. Significant different between different treatment groups were shown as *P

    Article Snippet: Cell lines and culture Normal human lung bronchial epithelial cells (NHBE) and NSCLC cell lines (A549 and H1299) were purchased from the ATCC (Manassas, USA).

    Techniques: Quantitative RT-PCR, Transfection, CCK-8 Assay

    FOXD3-AS1 repressed miR-127-3p expression in NSCLC cells. a Predicted binding sites between FOXD3-AS1 fragments and miR-127-3p. WT = wild type; MUT = mutated. b qRT-PCR determination of miR-127-3p expression in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. c , d Dual-luciferase reporter assay analysis of relative luciferase activity of reporter vector containing wild type or mutated FOXD3-AS1 fragment in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. e qRT-PCR determination of miR-127-3p expression in A549 cells transfected with pcDNA3.1, pcDNA3.1-FOXD3-AS1 (WT) or pcDNA3.1-FOXD3-AS1 (MUT). f RNA pull-down assay determined the interaction between FOXD3-AS1 and miR-127-3p. g qRT-PCR determination of miR-127-3p expression in A549/DDP cells with si-NC or si-FOXD3-AS1 transfection. h , i CCK-8 assay determination IC50 values (cisplatin) in A549/DDP cells with mimics NC or miR mimics transfection. j , k CCK-8 assay determination of IC50 values (cisplatin) in A549 cells with inhibitors NC or miR inhibitors transfection. l , m CCK-8 assay determination of IC50 values (cisplatin) in A549/DDP cells after being transfected with different oligonucleotides. Mimics NC = negative control for miR-127-3p mimics; miR mimics = miR-127-3p mimics; inhibitors NC = negative control for miR-127-3p inhibitors); miR inhibitors = miR-127-3p inhibitors. N = 3 biological samples, and each sample was assayed in triplicates. Significant differences between groups were shown as *P

    Journal: Cancer Cell International

    Article Title: LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis

    doi: 10.1186/s12935-020-01402-9

    Figure Lengend Snippet: FOXD3-AS1 repressed miR-127-3p expression in NSCLC cells. a Predicted binding sites between FOXD3-AS1 fragments and miR-127-3p. WT = wild type; MUT = mutated. b qRT-PCR determination of miR-127-3p expression in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. c , d Dual-luciferase reporter assay analysis of relative luciferase activity of reporter vector containing wild type or mutated FOXD3-AS1 fragment in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. e qRT-PCR determination of miR-127-3p expression in A549 cells transfected with pcDNA3.1, pcDNA3.1-FOXD3-AS1 (WT) or pcDNA3.1-FOXD3-AS1 (MUT). f RNA pull-down assay determined the interaction between FOXD3-AS1 and miR-127-3p. g qRT-PCR determination of miR-127-3p expression in A549/DDP cells with si-NC or si-FOXD3-AS1 transfection. h , i CCK-8 assay determination IC50 values (cisplatin) in A549/DDP cells with mimics NC or miR mimics transfection. j , k CCK-8 assay determination of IC50 values (cisplatin) in A549 cells with inhibitors NC or miR inhibitors transfection. l , m CCK-8 assay determination of IC50 values (cisplatin) in A549/DDP cells after being transfected with different oligonucleotides. Mimics NC = negative control for miR-127-3p mimics; miR mimics = miR-127-3p mimics; inhibitors NC = negative control for miR-127-3p inhibitors); miR inhibitors = miR-127-3p inhibitors. N = 3 biological samples, and each sample was assayed in triplicates. Significant differences between groups were shown as *P

    Article Snippet: Cell lines and culture Normal human lung bronchial epithelial cells (NHBE) and NSCLC cell lines (A549 and H1299) were purchased from the ATCC (Manassas, USA).

    Techniques: Expressing, Binding Assay, Quantitative RT-PCR, Transfection, Luciferase, Reporter Assay, Activity Assay, Plasmid Preparation, Pull Down Assay, CCK-8 Assay, Negative Control

    MiR-127-3p repressed MDM2 expression in NSCLC cells. a Predicted binding sites between miR-127-3p and MDM2 3′UTR. WT = wild type; MUT = mutated. b , c Dual-luciferase reporter assay analysis of relative luciferase activity of reporter vector containing wild type or mutated MDM2 3′UTR in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. d qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with mimics NC or miR mimics transfection. e qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with si-NC or si-FOXD3-AS1 expression. f qRT-PCR and western blot analysis of MDM2 expression in A549 cells with pcDNA3.1 or pcDNA3.1-MDM2 transfection. g , h CCK-8 assay analysis of IC50 values (cisplatin) in A549 cells with pcDNA3.1 or pcDNA3.1-MDM2 transfection. i qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with si-NC or si-MDM2 transfection. j , k CCK-8 assay analysis of IC50 values (cisplatin) in A549/DDP cells with si-NC or si-MDM2 transfection. l , m CCK-8 assay analysis of IC50 values (cisplatin) in A549/DDP cells after being transfected with different oligonucleotides. Mimics NC = negative control for miR-127-3p mimics; miR mimics = miR-127-3p mimics; inhibitors NC = negative control for miR-127-3p inhibitors); miR inhibitors = miR-127-3p inhibitors. N = 3 biological samples, and each sample was assayed in triplicates. Significant differences between groups were shown as *P

    Journal: Cancer Cell International

    Article Title: LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis

    doi: 10.1186/s12935-020-01402-9

    Figure Lengend Snippet: MiR-127-3p repressed MDM2 expression in NSCLC cells. a Predicted binding sites between miR-127-3p and MDM2 3′UTR. WT = wild type; MUT = mutated. b , c Dual-luciferase reporter assay analysis of relative luciferase activity of reporter vector containing wild type or mutated MDM2 3′UTR in A549/DDP cells with mimic NC, miR mimics, inhibitors NC or miR inhibitors transfection. d qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with mimics NC or miR mimics transfection. e qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with si-NC or si-FOXD3-AS1 expression. f qRT-PCR and western blot analysis of MDM2 expression in A549 cells with pcDNA3.1 or pcDNA3.1-MDM2 transfection. g , h CCK-8 assay analysis of IC50 values (cisplatin) in A549 cells with pcDNA3.1 or pcDNA3.1-MDM2 transfection. i qRT-PCR and western blot analysis of MDM2 expression in A549/DDP cells with si-NC or si-MDM2 transfection. j , k CCK-8 assay analysis of IC50 values (cisplatin) in A549/DDP cells with si-NC or si-MDM2 transfection. l , m CCK-8 assay analysis of IC50 values (cisplatin) in A549/DDP cells after being transfected with different oligonucleotides. Mimics NC = negative control for miR-127-3p mimics; miR mimics = miR-127-3p mimics; inhibitors NC = negative control for miR-127-3p inhibitors); miR inhibitors = miR-127-3p inhibitors. N = 3 biological samples, and each sample was assayed in triplicates. Significant differences between groups were shown as *P

    Article Snippet: Cell lines and culture Normal human lung bronchial epithelial cells (NHBE) and NSCLC cell lines (A549 and H1299) were purchased from the ATCC (Manassas, USA).

    Techniques: Expressing, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Plasmid Preparation, Transfection, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Negative Control

    FGTI-2734, but not FTI-2148 or GGTI-2418, inhibits both protein prenylation and membrane localization of KRAS and NRAS. A, Chemical structures and in vitro potency and selectivity of FTI-2148, GGTI-2418, and FGTI-2734. B , KRAS HRAS, and NRAS-transformed NIH3T3 cells were treated with vehicle (DMSO) or various concentrations of FGTI-2734, FTI-2148, and GGTI-2418 and processed for Western blotting with antibodies to KRAS, HRAS, NRAS, HDJ2, and RAP1A. Unprenylated bands of HDJ2, KRAS, HRAS, and NRAS show slower migration compared with fully prenylated HDJ2, KRAS, HRAS, and NRAS. RAP1A antibody can detect only unprenylated RAP1A. C , Human pancreatic cancer MiaPaCa2 and human lung cancer H460 cells were treated with vehicle (DMSO) or various concentrations of FGTI-2734, FTI-2148, and GGTI-2418, processed for membrane (P100) and cytosolic (S100) fractionation, and analyzed with Western blot using antibodies to KRAS, HRAS NRAS, and RAP1A. RHOGDI and IGF1R antibodies were used for internal controls for cytosolic and membrane fractions, respectively.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: Dual farnesyl and geranylgeranyl transferase inhibitor thwarts mutant KRAS-driven patient-derived pancreatic tumors

    doi: 10.1158/1078-0432.CCR-18-3399

    Figure Lengend Snippet: FGTI-2734, but not FTI-2148 or GGTI-2418, inhibits both protein prenylation and membrane localization of KRAS and NRAS. A, Chemical structures and in vitro potency and selectivity of FTI-2148, GGTI-2418, and FGTI-2734. B , KRAS HRAS, and NRAS-transformed NIH3T3 cells were treated with vehicle (DMSO) or various concentrations of FGTI-2734, FTI-2148, and GGTI-2418 and processed for Western blotting with antibodies to KRAS, HRAS, NRAS, HDJ2, and RAP1A. Unprenylated bands of HDJ2, KRAS, HRAS, and NRAS show slower migration compared with fully prenylated HDJ2, KRAS, HRAS, and NRAS. RAP1A antibody can detect only unprenylated RAP1A. C , Human pancreatic cancer MiaPaCa2 and human lung cancer H460 cells were treated with vehicle (DMSO) or various concentrations of FGTI-2734, FTI-2148, and GGTI-2418, processed for membrane (P100) and cytosolic (S100) fractionation, and analyzed with Western blot using antibodies to KRAS, HRAS NRAS, and RAP1A. RHOGDI and IGF1R antibodies were used for internal controls for cytosolic and membrane fractions, respectively.

    Article Snippet: Human lung cancer cell lines (A549, H460 and Calu6), colon cancer cell line (DLD1), and pancreatic cancer cell lines (MiaPaCa2, L3.6pl) were obtained from the ATCC (Manassas, VA, USA).

    Techniques: In Vitro, Transformation Assay, Western Blot, Migration, Fractionation

    FGTI-2734 induces apoptosis in mutant KRAS-dependent, but not independent, human cancer cell lines with different oncogenic KRAS mutation. A , mutant KRAS harboring MiaPaCa2, L3.6pl, and Calu6 (mutant KRAS-dependent cell lines). B , mutant KRAS harboring A549, H460, and DLD1 (mutant KRAS-independent cell lines). For both panels, cells were transiently infected with lentiviral guide RNAs (gRNA) of scrambled (SC) and KRAS gRNAs and treated with either vehicle (DMSO) or indicated concentrations of FGTI-2734 followed by Western blot analysis with indicated antibodies.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: Dual farnesyl and geranylgeranyl transferase inhibitor thwarts mutant KRAS-driven patient-derived pancreatic tumors

    doi: 10.1158/1078-0432.CCR-18-3399

    Figure Lengend Snippet: FGTI-2734 induces apoptosis in mutant KRAS-dependent, but not independent, human cancer cell lines with different oncogenic KRAS mutation. A , mutant KRAS harboring MiaPaCa2, L3.6pl, and Calu6 (mutant KRAS-dependent cell lines). B , mutant KRAS harboring A549, H460, and DLD1 (mutant KRAS-independent cell lines). For both panels, cells were transiently infected with lentiviral guide RNAs (gRNA) of scrambled (SC) and KRAS gRNAs and treated with either vehicle (DMSO) or indicated concentrations of FGTI-2734 followed by Western blot analysis with indicated antibodies.

    Article Snippet: Human lung cancer cell lines (A549, H460 and Calu6), colon cancer cell line (DLD1), and pancreatic cancer cell lines (MiaPaCa2, L3.6pl) were obtained from the ATCC (Manassas, VA, USA).

    Techniques: Mutagenesis, Infection, Western Blot

    Infection with influenza B virus induces faster IFN expression than infection with type A virus. (A) IFN-λ1 gene expression was analyzed in moDCs infected with influenza A/Beijing/353/89 and B/Shangdong/7/97 viruses at serial dilutions (MOIs of 125 to 0.2) for 16 h. (B) IFN-λ1 gene expression at different time points in A549 cells infected with the above-described viruses at an MOI of 2. (C) The same experiment was repeated with recombinant virus strains A/Udorn/307/72 and B/Yamagata/16/88 in moDCs at an MOI of 5, and IFN-λ1 gene expression was analyzed. All these experiments were repeated twice.

    Journal: Journal of Virology

    Article Title: Incoming Influenza A Virus Evades Early Host Recognition, while Influenza B Virus Induces Interferon Expression Directly upon Entry

    doi: 10.1128/JVI.01050-12

    Figure Lengend Snippet: Infection with influenza B virus induces faster IFN expression than infection with type A virus. (A) IFN-λ1 gene expression was analyzed in moDCs infected with influenza A/Beijing/353/89 and B/Shangdong/7/97 viruses at serial dilutions (MOIs of 125 to 0.2) for 16 h. (B) IFN-λ1 gene expression at different time points in A549 cells infected with the above-described viruses at an MOI of 2. (C) The same experiment was repeated with recombinant virus strains A/Udorn/307/72 and B/Yamagata/16/88 in moDCs at an MOI of 5, and IFN-λ1 gene expression was analyzed. All these experiments were repeated twice.

    Article Snippet: A549 human lung epithelial cells (ATCC CCL185), HEK293 human embryonic kidney cells (ATCC CLR1573), and Madin-Darby canine kidney (MDCK) cells (ATCC CCL34) were maintained with continuous growth in Eagle minimal essential medium (Eagle-MEM) (Sigma-Aldrich) supplemented with antibiotics, l -glutamine, HEPES, and 10% FCS.

    Techniques: Infection, Expressing, Recombinant

    Phospho-T99-glyceraldehyde 3-phosphate dehydrogenase was detected in nuclei of A549 cells after genotoxic stress. A: 2D gel analysis of the cytosolic fraction extracted from A549 cells. Only a section of the membrane containing GAPDH isoforms is shown.

    Journal: World Journal of Biological Chemistry

    Article Title: Disruption of NAD+ binding site in glyceraldehyde 3-phosphate dehydrogenase affects its intranuclear interactions

    doi: 10.4331/wjbc.v6.i4.366

    Figure Lengend Snippet: Phospho-T99-glyceraldehyde 3-phosphate dehydrogenase was detected in nuclei of A549 cells after genotoxic stress. A: 2D gel analysis of the cytosolic fraction extracted from A549 cells. Only a section of the membrane containing GAPDH isoforms is shown.

    Article Snippet: Lung carcinoma cells A549 were obtained from the ATCC collection (ATCC, Manassas, VA).

    Techniques: Two-Dimensional Gel Electrophoresis

    The tandem mass spectrometry (MS/MS) profile of glyceraldehyde 3-phosphate dehydrogenase peptides. Proteomics characterization of a basic GAPDH isoform (spot 1 from Figure ) from the cytosolic fraction of A549 cells by mass spectroscopy.

    Journal: World Journal of Biological Chemistry

    Article Title: Disruption of NAD+ binding site in glyceraldehyde 3-phosphate dehydrogenase affects its intranuclear interactions

    doi: 10.4331/wjbc.v6.i4.366

    Figure Lengend Snippet: The tandem mass spectrometry (MS/MS) profile of glyceraldehyde 3-phosphate dehydrogenase peptides. Proteomics characterization of a basic GAPDH isoform (spot 1 from Figure ) from the cytosolic fraction of A549 cells by mass spectroscopy.

    Article Snippet: Lung carcinoma cells A549 were obtained from the ATCC collection (ATCC, Manassas, VA).

    Techniques: Mass Spectrometry

    Glyceraldehyde 3-phosphate dehydrogenase isoforms in A549 cells. A: 2D gel separation (pH range 3-11) of proteins from the nuclear (NE) and the cytosolic (CE) fraction of A549 cells after 1 μmol/L araC treatment for 24 h. The membrane was developed

    Journal: World Journal of Biological Chemistry

    Article Title: Disruption of NAD+ binding site in glyceraldehyde 3-phosphate dehydrogenase affects its intranuclear interactions

    doi: 10.4331/wjbc.v6.i4.366

    Figure Lengend Snippet: Glyceraldehyde 3-phosphate dehydrogenase isoforms in A549 cells. A: 2D gel separation (pH range 3-11) of proteins from the nuclear (NE) and the cytosolic (CE) fraction of A549 cells after 1 μmol/L araC treatment for 24 h. The membrane was developed

    Article Snippet: Lung carcinoma cells A549 were obtained from the ATCC collection (ATCC, Manassas, VA).

    Techniques: Two-Dimensional Gel Electrophoresis

    Replication patterns observed in A549 cells under standard conditions, and the numbers of replication foci in the absence and presence of replication stress induced by camptothecin. ( A ) changes of the pattern of replication foci visualized in live cells

    Journal: Cell Cycle

    Article Title: Activation of new replication foci under conditions of replication stress

    doi: 10.1080/15384101.2015.1064566

    Figure Lengend Snippet: Replication patterns observed in A549 cells under standard conditions, and the numbers of replication foci in the absence and presence of replication stress induced by camptothecin. ( A ) changes of the pattern of replication foci visualized in live cells

    Article Snippet: A549 human lung adenocarcinoma cells were obtained from ATCC and cultured in Nutrient Mixture Ham F-12 (Sigma-Aldrich, cat. no. N6760) supplemented with 10% fetal bovine serum (Sigma-Aldrich, cat. no. F2442) and antibiotics.

    Techniques:

    eFluxx-ID® MDR probes detect all three major types of ABC transporters in a similar manner as doxorubicin and mitoxantrone probes, but are significantly brighter, providing much higher sensitivity compared with the other dyes. Model cell lines (CHO K1, panel A, and A549, panel B) were trypsinized, washed with PBS, aliquoted at 5×10 5 cells/sample, and treated in triplicates with different inhibitors (5 µM of cyclosporin A, 20 µM of verapamil, 50 µM of MK-571, or 0.05 µM of novobiocin) or left untreated. Tested probes (eFluxx-ID® Green, eFluxx-ID® Gold dyes, doxorubicin or mitoxantrone) were added to every sample. The cells were incubated with the dye(s) in the presence or absence of inhibitors for 30 min at 37°C. Then cells were immediately analyzed by flow cytometry. Population comparison was performed using Kolmogorov-Smirnov statistics [26] . Clear histograms represent sample fluorescence in the presence of the inhibitor, shaded – without the inhibitor. The numbers indicate average D-values for each sample from at least three independent experiments, with SD not exceeding 10% for each value.

    Journal: PLoS ONE

    Article Title: Sensitive and Specific Fluorescent Probes for Functional Analysis of the Three Major Types of Mammalian ABC Transporters

    doi: 10.1371/journal.pone.0022429

    Figure Lengend Snippet: eFluxx-ID® MDR probes detect all three major types of ABC transporters in a similar manner as doxorubicin and mitoxantrone probes, but are significantly brighter, providing much higher sensitivity compared with the other dyes. Model cell lines (CHO K1, panel A, and A549, panel B) were trypsinized, washed with PBS, aliquoted at 5×10 5 cells/sample, and treated in triplicates with different inhibitors (5 µM of cyclosporin A, 20 µM of verapamil, 50 µM of MK-571, or 0.05 µM of novobiocin) or left untreated. Tested probes (eFluxx-ID® Green, eFluxx-ID® Gold dyes, doxorubicin or mitoxantrone) were added to every sample. The cells were incubated with the dye(s) in the presence or absence of inhibitors for 30 min at 37°C. Then cells were immediately analyzed by flow cytometry. Population comparison was performed using Kolmogorov-Smirnov statistics [26] . Clear histograms represent sample fluorescence in the presence of the inhibitor, shaded – without the inhibitor. The numbers indicate average D-values for each sample from at least three independent experiments, with SD not exceeding 10% for each value.

    Article Snippet: Cell lines Human cervical adenocarcinoma epithelial cell line HeLa (putative MDR negative cell line), human lung carcinoma cell line A549 (expression of MPR1 and BCRP , ) and hamster ovary CHO K1 cell line (expression of all three major ABC transporter proteins , ) were obtained from ATCC (Manassas, VA).

    Techniques: Incubation, Flow Cytometry, Cytometry, Fluorescence

    A–D. CHO K1 and A549 cell lines display increased chemoresistance toward the cytotoxic drugs that are mostly associated with MDR: doxorubicin (panel A), taxol (panel B), vincristine (panel C), and mitoxantrone (panel D). The U-2 OS cell line demonstrates moderately increased chemoresistance to a few drugs associated to MDR, such as doxorubicin (panel A) and mitoxantrone (panel D). The HeLa cell line was used as a non-chemoresistant control specimen. Cells were seeded in 96 well plates, treated with the different doses of indicated drugs, and a standard MTT viability test was performed 1 and 2 days post-treatment. Results are presented as a ratio of the OD 595 of treated cells to the OD 595 of the untreated cells.

    Journal: PLoS ONE

    Article Title: Sensitive and Specific Fluorescent Probes for Functional Analysis of the Three Major Types of Mammalian ABC Transporters

    doi: 10.1371/journal.pone.0022429

    Figure Lengend Snippet: A–D. CHO K1 and A549 cell lines display increased chemoresistance toward the cytotoxic drugs that are mostly associated with MDR: doxorubicin (panel A), taxol (panel B), vincristine (panel C), and mitoxantrone (panel D). The U-2 OS cell line demonstrates moderately increased chemoresistance to a few drugs associated to MDR, such as doxorubicin (panel A) and mitoxantrone (panel D). The HeLa cell line was used as a non-chemoresistant control specimen. Cells were seeded in 96 well plates, treated with the different doses of indicated drugs, and a standard MTT viability test was performed 1 and 2 days post-treatment. Results are presented as a ratio of the OD 595 of treated cells to the OD 595 of the untreated cells.

    Article Snippet: Cell lines Human cervical adenocarcinoma epithelial cell line HeLa (putative MDR negative cell line), human lung carcinoma cell line A549 (expression of MPR1 and BCRP , ) and hamster ovary CHO K1 cell line (expression of all three major ABC transporter proteins , ) were obtained from ATCC (Manassas, VA).

    Techniques: MTT Assay

    Influence of recombinant NanA and NanB on expression of SA on the surface of A549 cells . Cells were treated with different neuraminidase dilutions for 48 h. The lectins MAA (A) and SNA (B) were used to detect SAα2-3Gal and SAα2-6Gal, respectively, by immunocytochemical staining. Control (Co) was stained without using lectins.

    Journal: Frontiers in Microbiology

    Article Title: Dual Acting Neuraminidase Inhibitors Open New Opportunities to Disrupt the Lethal Synergism between Streptococcus pneumoniae and Influenza Virus

    doi: 10.3389/fmicb.2016.00357

    Figure Lengend Snippet: Influence of recombinant NanA and NanB on expression of SA on the surface of A549 cells . Cells were treated with different neuraminidase dilutions for 48 h. The lectins MAA (A) and SNA (B) were used to detect SAα2-3Gal and SAα2-6Gal, respectively, by immunocytochemical staining. Control (Co) was stained without using lectins.

    Article Snippet: Test medium used for virus propagation and in vitro studies with virus was serum-free but contained 0.25 μg/mL (A549 cells) or 2 μg/mL (MDCK cells) trypsin (Sigma–Aldrich GmbH) and 1.3% sodium bicarbonate (Lonza Group Ltd.).

    Techniques: Recombinant, Expressing, Staining

    Spread of A(H1N1)pdm09 strain A/Jena/8178/09 (Jena/8178) in the absence and the presence of different dilutions of recombinant NanA and NanB . The effect of NanA (A) and NanB (B) on virus spread in A549 cells was analyzed by immunocytochemical staining of viral nucleoprotein (shown in red) 48 h after infection with Jena/8178 at MOI of 0.1 TCID 50 /cell.

    Journal: Frontiers in Microbiology

    Article Title: Dual Acting Neuraminidase Inhibitors Open New Opportunities to Disrupt the Lethal Synergism between Streptococcus pneumoniae and Influenza Virus

    doi: 10.3389/fmicb.2016.00357

    Figure Lengend Snippet: Spread of A(H1N1)pdm09 strain A/Jena/8178/09 (Jena/8178) in the absence and the presence of different dilutions of recombinant NanA and NanB . The effect of NanA (A) and NanB (B) on virus spread in A549 cells was analyzed by immunocytochemical staining of viral nucleoprotein (shown in red) 48 h after infection with Jena/8178 at MOI of 0.1 TCID 50 /cell.

    Article Snippet: Test medium used for virus propagation and in vitro studies with virus was serum-free but contained 0.25 μg/mL (A549 cells) or 2 μg/mL (MDCK cells) trypsin (Sigma–Aldrich GmbH) and 1.3% sodium bicarbonate (Lonza Group Ltd.).

    Techniques: Recombinant, Staining, Infection

    Inhibition of replication of A(H1N1)pdm09 strain A/Jena/8178/09 (Jena/8178) by neuraminidase inhibitors (NAIs) . A549 cells infected with Jena/8178 (MOI of 0.1 TCID 50 /cells) were treated with oseltamivir, zanamivir, DANA, artocarpin, and katsumadain A in absence of pneumococcal NAs (A) , presence of rNanA (B) or presence of rNanB (C) . Virus-infected cells were detected by immunocytochemical staining of viral nucleoprotein (shown in red) 48 h after infection to visualize the inhibitor effect on virus spread. To analyze the effect of NAIs on virus yield (D) , virus titers in pfu/mL were determined with plaque assay 48 h after infection. Virus control titer was set to 100% and inhibition of the control titer by NAIs in % was calculated. Experiments were performed at least three times, and one representative assay is exemplarily shown. Significant values were calculated with non-parametric Wilcoxon–Mann–Whitney test ( ∗ p

    Journal: Frontiers in Microbiology

    Article Title: Dual Acting Neuraminidase Inhibitors Open New Opportunities to Disrupt the Lethal Synergism between Streptococcus pneumoniae and Influenza Virus

    doi: 10.3389/fmicb.2016.00357

    Figure Lengend Snippet: Inhibition of replication of A(H1N1)pdm09 strain A/Jena/8178/09 (Jena/8178) by neuraminidase inhibitors (NAIs) . A549 cells infected with Jena/8178 (MOI of 0.1 TCID 50 /cells) were treated with oseltamivir, zanamivir, DANA, artocarpin, and katsumadain A in absence of pneumococcal NAs (A) , presence of rNanA (B) or presence of rNanB (C) . Virus-infected cells were detected by immunocytochemical staining of viral nucleoprotein (shown in red) 48 h after infection to visualize the inhibitor effect on virus spread. To analyze the effect of NAIs on virus yield (D) , virus titers in pfu/mL were determined with plaque assay 48 h after infection. Virus control titer was set to 100% and inhibition of the control titer by NAIs in % was calculated. Experiments were performed at least three times, and one representative assay is exemplarily shown. Significant values were calculated with non-parametric Wilcoxon–Mann–Whitney test ( ∗ p

    Article Snippet: Test medium used for virus propagation and in vitro studies with virus was serum-free but contained 0.25 μg/mL (A549 cells) or 2 μg/mL (MDCK cells) trypsin (Sigma–Aldrich GmbH) and 1.3% sodium bicarbonate (Lonza Group Ltd.).

    Techniques: Inhibition, Infection, Staining, Plaque Assay, MANN-WHITNEY

    MTT assays. A549 cells were treated with increasing concentration of XAV939 (0.1, 0.5, 1,5 and 10 µM) for 24, 4, 72 and 96 h. The result was shown as relative cell viability per concentration at each time point.

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: MTT assays. A549 cells were treated with increasing concentration of XAV939 (0.1, 0.5, 1,5 and 10 µM) for 24, 4, 72 and 96 h. The result was shown as relative cell viability per concentration at each time point.

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: MTT Assay, Concentration Assay

    Localization of β-catenin immunofluorescence in response to treatment with NaCl (control), 0., 1 and 10 µmol/l XAV939 in A549 cells (magnification, ×400).

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: Localization of β-catenin immunofluorescence in response to treatment with NaCl (control), 0., 1 and 10 µmol/l XAV939 in A549 cells (magnification, ×400).

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: Immunofluorescence

    c-Myc mRNA expression at different XAV939 concentrations as detected by RT-sqPCR. (A) RT-PCR gel (B) and relative expression of β-catenin mRNA in A549 cells, treated with different XAV939 concentrations. *P

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: c-Myc mRNA expression at different XAV939 concentrations as detected by RT-sqPCR. (A) RT-PCR gel (B) and relative expression of β-catenin mRNA in A549 cells, treated with different XAV939 concentrations. *P

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

    Εffect of XAV939 on A549 cell migration was detected via wound-healing assay. The wound widths in the different XAV939 treatment groups (0.1, 0.5, 1, 5, 10 µmol/l) after 24 h were all significantly wider than those of the control group (magnification, ×200).

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: Εffect of XAV939 on A549 cell migration was detected via wound-healing assay. The wound widths in the different XAV939 treatment groups (0.1, 0.5, 1, 5, 10 µmol/l) after 24 h were all significantly wider than those of the control group (magnification, ×200).

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: Migration, Wound Healing Assay

    β-catenin mRNA expression at different XAV939 concentrations as detected by RT-sqPCR. (A) RT-PCR gel (B) and relative expression of β-catenin mRNA in A549 cells, treated with different XAV939 concentrations. *P

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: β-catenin mRNA expression at different XAV939 concentrations as detected by RT-sqPCR. (A) RT-PCR gel (B) and relative expression of β-catenin mRNA in A549 cells, treated with different XAV939 concentrations. *P

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

    (A) XAV939 inhibits the clonogenicity of A549 cells in vitro . (B) Treatment of the A549 cell line with 0.1, 1 and 10 µmol/l XAV939 significantly inhibited colony formation compared with the control. *P

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: (A) XAV939 inhibits the clonogenicity of A549 cells in vitro . (B) Treatment of the A549 cell line with 0.1, 1 and 10 µmol/l XAV939 significantly inhibited colony formation compared with the control. *P

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: In Vitro

    Expression of TNKS in three lung adenocarcinoma cell lines. (A) Western blot analysis and (B) quantification of this analysis demonstrated that the level of TNKS protein expression in A549 cells was significantly higher compared with that in Calu-3 and SK-LU-1 cells. *P

    Journal: Oncology Letters

    Article Title: XAV939 inhibits the proliferation and migration of lung adenocarcinoma A549 cells through the WNT pathway

    doi: 10.3892/ol.2018.8491

    Figure Lengend Snippet: Expression of TNKS in three lung adenocarcinoma cell lines. (A) Western blot analysis and (B) quantification of this analysis demonstrated that the level of TNKS protein expression in A549 cells was significantly higher compared with that in Calu-3 and SK-LU-1 cells. *P

    Article Snippet: A549 cells treated with XAV939 or DDP exhibited decreased the expression of TNKS protein compared with untreated control cells. c-Myc, a downstream target of β-catenin, was also downregulated.

    Techniques: Expressing, Western Blot

    Effects of trichostatin A (TSA) alone or in combination with quercetin on the growth (A) and apoptosis (B) of A549 cells and H1299 cells. The cells were incubated with TSA (25 ng/mL) alone or in combination with 2 or 5 µM quercetin (2Q and 5Q, respectively) for 24 h and 48 h. Values (means ± SD, n = 3) at the same time not sharing a common letter (a-c and A-C for 24 and 48 h, respectively) are significantly different ( p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: Effects of trichostatin A (TSA) alone or in combination with quercetin on the growth (A) and apoptosis (B) of A549 cells and H1299 cells. The cells were incubated with TSA (25 ng/mL) alone or in combination with 2 or 5 µM quercetin (2Q and 5Q, respectively) for 24 h and 48 h. Values (means ± SD, n = 3) at the same time not sharing a common letter (a-c and A-C for 24 and 48 h, respectively) are significantly different ( p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Incubation

    Effects of trichostatin A (TSA) alone or in combination with quercetin on tumor growth (A); p53 protein expression in tumor tissue determined by immunohistochemical (IHC) staining (B) and western blot (C); and the level of apoptosis in tumor tissue determined by TUNEL assay (D) in tumor-bearing mice. Thirty male nude mice at age 5 weeks were injected with A549 cells and after 4 weeks were treated for 13 weeks with TSA (low dose, 0.5 mg/kg body weight; high dose, 1 mg/kg body weight), or quercetin alone or combined as described in the Methods . The control group was administered the vehicle only. At the end of the experiment, the mice were sacrificed and tumor tissues were analyzed for p53 protein expression and apoptosis. Values (means ± SD, n = 6) not sharing a common letter (a-d) are significantly different (p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: Effects of trichostatin A (TSA) alone or in combination with quercetin on tumor growth (A); p53 protein expression in tumor tissue determined by immunohistochemical (IHC) staining (B) and western blot (C); and the level of apoptosis in tumor tissue determined by TUNEL assay (D) in tumor-bearing mice. Thirty male nude mice at age 5 weeks were injected with A549 cells and after 4 weeks were treated for 13 weeks with TSA (low dose, 0.5 mg/kg body weight; high dose, 1 mg/kg body weight), or quercetin alone or combined as described in the Methods . The control group was administered the vehicle only. At the end of the experiment, the mice were sacrificed and tumor tissues were analyzed for p53 protein expression and apoptosis. Values (means ± SD, n = 6) not sharing a common letter (a-d) are significantly different (p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Expressing, Immunohistochemistry, Staining, Western Blot, TUNEL Assay, Mouse Assay, Injection

    Effects of trichostatin A (TSA) alone or in combination with quercetin on Bax, Apaf-1 and Bcl-2 protein expression in A 549 cell without or with p53-silencing (A); cytochrome c levels in cytosol and mitochondria in A549 cells without p53-silencing (B). The A549 cells were transfected with or without p53 siRNA before incubation with TSA (25 ng/mL) alone or in combination with 5 µM quercetin (5Q) for 18 h. Values (means ± SD, n = 3) among the groups without p53-silencing not sharing a common letter (a-c) are significantly different ( p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: Effects of trichostatin A (TSA) alone or in combination with quercetin on Bax, Apaf-1 and Bcl-2 protein expression in A 549 cell without or with p53-silencing (A); cytochrome c levels in cytosol and mitochondria in A549 cells without p53-silencing (B). The A549 cells were transfected with or without p53 siRNA before incubation with TSA (25 ng/mL) alone or in combination with 5 µM quercetin (5Q) for 18 h. Values (means ± SD, n = 3) among the groups without p53-silencing not sharing a common letter (a-c) are significantly different ( p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Expressing, Transfection, Incubation

    Effects of trichostatin A (TSA) alone or in combination with quercetin on the expression of acetyl histone H3 (acetyl H3) and H4 (acetyl H4) in A549 cells without (A) or with (B) p53 siRNA transfection. The cells were incubated with TSA (25 ng/mL) alone or in combination with 5 µM quercetin (5Q) for 24 or 48 h. Values (means ± SD, n = 3) not sharing a common letter (a-c) are significantly different ( p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: Effects of trichostatin A (TSA) alone or in combination with quercetin on the expression of acetyl histone H3 (acetyl H3) and H4 (acetyl H4) in A549 cells without (A) or with (B) p53 siRNA transfection. The cells were incubated with TSA (25 ng/mL) alone or in combination with 5 µM quercetin (5Q) for 24 or 48 h. Values (means ± SD, n = 3) not sharing a common letter (a-c) are significantly different ( p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Expressing, Transfection, Incubation

    p53 protein expression in A549 cells without (A) or with (B) p53 siRNA transfection and the effect of p53 siRNA transfection on apoptosis (C) induced by various treatments. The A549 cells were transfected with or without p53 siRNA before incubation with 25 ng/mL trichostatin A (TSA) alone or in combination with 5 µM quercetin (5Q) for 12 h or 48 h for the p53 expression assay and apoptosis assay, respectively. Values (mean ± SD) in the same group not sharing a common letter (a-c and A-C for without or with p53 siRNA, respectively) are significantly different ( p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: p53 protein expression in A549 cells without (A) or with (B) p53 siRNA transfection and the effect of p53 siRNA transfection on apoptosis (C) induced by various treatments. The A549 cells were transfected with or without p53 siRNA before incubation with 25 ng/mL trichostatin A (TSA) alone or in combination with 5 µM quercetin (5Q) for 12 h or 48 h for the p53 expression assay and apoptosis assay, respectively. Values (mean ± SD) in the same group not sharing a common letter (a-c and A-C for without or with p53 siRNA, respectively) are significantly different ( p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Expressing, Transfection, Incubation, Apoptosis Assay

    Effects of trichostatin A (TSA) alone or in combination with quercetin on caspase-9 (A) and caspase-3 activity (B) in A549 cells with or without p53-silencing. The A549 cells were transfected with or without p53 siRNA before incubation with 25 ng/mL TSA alone or in combination with 5 µM quercetin (5Q) for 24 h. Values (means ± SD, n = 3) among the groups without p53-silencing not sharing a common letter (a-c) are significantly different ( p

    Journal: PLoS ONE

    Article Title: Quercetin Enhances the Antitumor Activity of Trichostatin A through Upregulation of p53 Protein Expression In Vitro and In Vivo

    doi: 10.1371/journal.pone.0054255

    Figure Lengend Snippet: Effects of trichostatin A (TSA) alone or in combination with quercetin on caspase-9 (A) and caspase-3 activity (B) in A549 cells with or without p53-silencing. The A549 cells were transfected with or without p53 siRNA before incubation with 25 ng/mL TSA alone or in combination with 5 µM quercetin (5Q) for 24 h. Values (means ± SD, n = 3) among the groups without p53-silencing not sharing a common letter (a-c) are significantly different ( p

    Article Snippet: After being acclimated for 1 week, the animals were subcutaneously injected in the right flank with A549 cells at a dose of 5×106 cells (in 200 µL of matrigel; BD Biosciences, Franklin Lakes, NJ, USA).

    Techniques: Activity Assay, Transfection, Incubation

    Young’s modulus values expressed in kPa, calculated from the nuclear region and the cytoskeletal area of Caco-2 ( a ) and A549 ( b ) cell lines after a treatment to 45 μg/ml of SiO 2 NPs and TiO 2 NPs for 72 h

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: Young’s modulus values expressed in kPa, calculated from the nuclear region and the cytoskeletal area of Caco-2 ( a ) and A549 ( b ) cell lines after a treatment to 45 μg/ml of SiO 2 NPs and TiO 2 NPs for 72 h

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques:

    Integrated density ( a , b ) and coherency ( c , d ) for Caco-2 and A549 cells treated with 45 μg/ml of SiO 2 NPs and TiO 2 NPs after 72 h. The integrated density and coherency values were expressed as a mean value and relative SD, calculated from confocal acquisitions by ImageJ (calculation on 15 cells). The mean values and their standard deviations were reported in the histograms. Results were statistically significant for p

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: Integrated density ( a , b ) and coherency ( c , d ) for Caco-2 and A549 cells treated with 45 μg/ml of SiO 2 NPs and TiO 2 NPs after 72 h. The integrated density and coherency values were expressed as a mean value and relative SD, calculated from confocal acquisitions by ImageJ (calculation on 15 cells). The mean values and their standard deviations were reported in the histograms. Results were statistically significant for p

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques:

    a – d SOD and MDA assays on Caco-2 and A549 cells. Cells were incubated with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, 96 h. The SOD assay used a tetrazolium salt for detection of superoxide radicals generated by xanthine oxidase and hypoxanthine. The standard curve was used as a positive control (data not shown). The MDA levels was detected by the quantification of MDA-TBA adduct (OD = 532 nm). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: a – d SOD and MDA assays on Caco-2 and A549 cells. Cells were incubated with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, 96 h. The SOD assay used a tetrazolium salt for detection of superoxide radicals generated by xanthine oxidase and hypoxanthine. The standard curve was used as a positive control (data not shown). The MDA levels was detected by the quantification of MDA-TBA adduct (OD = 532 nm). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques: Multiple Displacement Amplification, Incubation, Generated, Positive Control

    Local enlargement of confocal acquisitions acquired in Figs. 6 and 7 showed (more in details) the effect of SiO 2 NPS and TiO 2 NPs on actin network of Caco-2 and A549 cells after the exposure of 45 μg/ml of NPs for 72 h and 96 h

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: Local enlargement of confocal acquisitions acquired in Figs. 6 and 7 showed (more in details) the effect of SiO 2 NPS and TiO 2 NPs on actin network of Caco-2 and A549 cells after the exposure of 45 μg/ml of NPs for 72 h and 96 h

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques:

    Effect of SiO 2 NPS and TiO 2 NPs on actin network on A549 cells. A549 were treated with 15 μg/ml and 45 μg/ml of NPs for 24 h, 48 h, 72 h, and 96 h; successively they were fixed and stained with Phalloidin–ATTO 488 and DAPI. The 2D images of cortical actin were acquired by a Zeiss LSM700 (Zeiss) confocal microscope equipped with an Axio Observer Z1 (Zeiss) inverted microscope using a × 100, 1.46 numerical aperture oil immersion lens. All data were processed by ZEN software (Zeiss)

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: Effect of SiO 2 NPS and TiO 2 NPs on actin network on A549 cells. A549 were treated with 15 μg/ml and 45 μg/ml of NPs for 24 h, 48 h, 72 h, and 96 h; successively they were fixed and stained with Phalloidin–ATTO 488 and DAPI. The 2D images of cortical actin were acquired by a Zeiss LSM700 (Zeiss) confocal microscope equipped with an Axio Observer Z1 (Zeiss) inverted microscope using a × 100, 1.46 numerical aperture oil immersion lens. All data were processed by ZEN software (Zeiss)

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques: Staining, Microscopy, Inverted Microscopy, Software

    TiO 2 NPs and SiO 2 NPs accumulation in Caco-2 and A549 cell lines exposed to 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h. Cells were then harvested, live cells were counted, and Ti and Si content was measured in 360,000 cells (μg Ti and μg Si). Data reported as mean ± SD from three independent experiments; statistical significance of exposed cells vs. control cells for p value

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: TiO 2 NPs and SiO 2 NPs accumulation in Caco-2 and A549 cell lines exposed to 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h. Cells were then harvested, live cells were counted, and Ti and Si content was measured in 360,000 cells (μg Ti and μg Si). Data reported as mean ± SD from three independent experiments; statistical significance of exposed cells vs. control cells for p value

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques:

    LDH ( a – b ) and ROS ( c – d ) assays on Caco-2 and A549 cells. Cells were incubated with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h. Percent of LDH leakage of nanoparticle-treated cells are expressed relative to non-treated control cells. Positive controls (P) consisted in the treatment of cells with 0.9% Triton X-100 showing ca. 500% LDH increase (data not shown). ROS levels were recorded exposing Caco-2 and A549 cells with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h incubated with 100 μM DCFH-DA. Cell fluorescence was measured. As a positive control (P), cells were incubated with 500 μM H 2 O 2 showing a ca. 300% DCFH-DA increase (not show). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: LDH ( a – b ) and ROS ( c – d ) assays on Caco-2 and A549 cells. Cells were incubated with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h. Percent of LDH leakage of nanoparticle-treated cells are expressed relative to non-treated control cells. Positive controls (P) consisted in the treatment of cells with 0.9% Triton X-100 showing ca. 500% LDH increase (data not shown). ROS levels were recorded exposing Caco-2 and A549 cells with 15 μg/ml and 45 μg/ml of TiO 2 NPs and SiO 2 NPs for 24 h, 48 h, 72 h, and 96 h incubated with 100 μM DCFH-DA. Cell fluorescence was measured. As a positive control (P), cells were incubated with 500 μM H 2 O 2 showing a ca. 300% DCFH-DA increase (not show). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques: Incubation, Fluorescence, Positive Control

    Viability assay (WST-8) of Caco-2 ( a ) and A549 ( b ) cells after 24 h, 48 h, 72 h, and 96 h of exposure to two doses (15 μg/ml and 45 μg/ml) of TiO 2 NPs and SiO 2 NPs. Viability of NP-treated cells was normalized to non-treated control cells. As positive control (P), cells were incubated with 5% DMSO (data not shown). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Journal: Nanoscale Research Letters

    Article Title: Tailoring Cell Morphomechanical Perturbations Through Metal Oxide Nanoparticles

    doi: 10.1186/s11671-019-2941-y

    Figure Lengend Snippet: Viability assay (WST-8) of Caco-2 ( a ) and A549 ( b ) cells after 24 h, 48 h, 72 h, and 96 h of exposure to two doses (15 μg/ml and 45 μg/ml) of TiO 2 NPs and SiO 2 NPs. Viability of NP-treated cells was normalized to non-treated control cells. As positive control (P), cells were incubated with 5% DMSO (data not shown). Data reported as mean ± SD from three independent experiments are considered statistically significant compared with control ( n = 8) for p value

    Article Snippet: AFM Analysis Caco-2 and A549 cells were seeded in plastic Petri dishes (Corning) at a concentration of 105 cell/well and grown until a 70–80% of confluence.

    Techniques: Viability Assay, Positive Control, Incubation

    Radiosensitizing effects of miR‐18a‐5p in vivo under irradiation. A, Growth curves of A549 xenografts at day 10 (n = 6, P

    Journal: Cancer Medicine

    Article Title: Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α, et al. Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α

    doi: 10.1002/cam4.1527

    Figure Lengend Snippet: Radiosensitizing effects of miR‐18a‐5p in vivo under irradiation. A, Growth curves of A549 xenografts at day 10 (n = 6, P

    Article Snippet: The results showed that miR‐18a‐5p was more highly expressed in A549 cells than in HBE cells (Figure A).

    Techniques: In Vivo, Irradiation

    Radiosensitizing effects of miR‐18a‐5p on A549 cells. A, miR‐18a‐5p expression in HBE and A549 cells (** P

    Journal: Cancer Medicine

    Article Title: Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α, et al. Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α

    doi: 10.1002/cam4.1527

    Figure Lengend Snippet: Radiosensitizing effects of miR‐18a‐5p on A549 cells. A, miR‐18a‐5p expression in HBE and A549 cells (** P

    Article Snippet: The results showed that miR‐18a‐5p was more highly expressed in A549 cells than in HBE cells (Figure A).

    Techniques: Expressing

    Radiosensitizing effects of miR‐18a‐5p on CD 133 + cells. A, The proportion of CD 133 + stem‐like cells in parent A549 cells and A549 cells induced into spheres. B, mRNA expression of stemness factors (Oct4, Nestin, Nanog) in CD 133‐ and stem‐like CD 133 + cells (** P

    Journal: Cancer Medicine

    Article Title: Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α, et al. Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α

    doi: 10.1002/cam4.1527

    Figure Lengend Snippet: Radiosensitizing effects of miR‐18a‐5p on CD 133 + cells. A, The proportion of CD 133 + stem‐like cells in parent A549 cells and A549 cells induced into spheres. B, mRNA expression of stemness factors (Oct4, Nestin, Nanog) in CD 133‐ and stem‐like CD 133 + cells (** P

    Article Snippet: The results showed that miR‐18a‐5p was more highly expressed in A549 cells than in HBE cells (Figure A).

    Techniques: Expressing