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non small cell lung cancer cell lines pc 9  (ATCC)


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    Structured Review

    ATCC non small cell lung cancer cell lines pc 9
    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
    Non Small Cell Lung Cancer Cell Lines Pc 9, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 31317 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 31317 article reviews
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    1) Product Images from "ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response"

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2026.102568

    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
    Figure Legend Snippet: IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Techniques Used: Concentration Assay, CRISPR

    Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
    Figure Legend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Techniques Used: Inhibition, Expressing, Control

    Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.
    Figure Legend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Techniques Used: Inhibition



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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    ATCC non small cell lung cancer cell line pc 9
    Spironolactone selectively induces cell death and inhibits the growth of cancer cells. <t>A549,</t> PANC-1, PC-9, and PC-9-OR (osimertinib-resistant) ( a ), cancer stem cell lines (A549 CSLC and PANC-1 CSLC) ( b ), and IMR90 normal human fibroblasts ( c ) were treated without (as control) or with the indicated concentrations of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panels) as well as the percentage of dead cells (right panels) were then assessed. Values in the graphs represent the means ± SD of triplicate samples of a representative experiment repeated with similar results. * p < 0.05.
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    Image Search Results


    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Concentration Assay, CRISPR

    Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Inhibition, Expressing, Control

    Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Inhibition

    Spironolactone selectively induces cell death and inhibits the growth of cancer cells. A549, PANC-1, PC-9, and PC-9-OR (osimertinib-resistant) ( a ), cancer stem cell lines (A549 CSLC and PANC-1 CSLC) ( b ), and IMR90 normal human fibroblasts ( c ) were treated without (as control) or with the indicated concentrations of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panels) as well as the percentage of dead cells (right panels) were then assessed. Values in the graphs represent the means ± SD of triplicate samples of a representative experiment repeated with similar results. * p < 0.05.

    Journal: Cancers

    Article Title: Spironolactone, a Classic Potassium-Sparing Diuretic, Reduces Survivin Expression and Chemosensitizes Cancer Cells to Non-DNA-Damaging Anticancer Drugs

    doi: 10.3390/cancers11101550

    Figure Lengend Snippet: Spironolactone selectively induces cell death and inhibits the growth of cancer cells. A549, PANC-1, PC-9, and PC-9-OR (osimertinib-resistant) ( a ), cancer stem cell lines (A549 CSLC and PANC-1 CSLC) ( b ), and IMR90 normal human fibroblasts ( c ) were treated without (as control) or with the indicated concentrations of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panels) as well as the percentage of dead cells (right panels) were then assessed. Values in the graphs represent the means ± SD of triplicate samples of a representative experiment repeated with similar results. * p < 0.05.

    Article Snippet: The human non-small cell lung cancer (NSCLC) cell lines A549 and PC-9 were obtained from the Riken BioResource Center (Tsukuba, Japan).

    Techniques: Control

    Spironolactone decreases survivin expression and survivin reductions imitate the chemosensitizing effects of spironolactone. Cells treated with or without 25 µM spironolactone (SPL) for three days were subjected to an immunoblot analysis for survivin expression ( a , b ). YM155, a pharmacological survivin inhibitor, at the concentration of 10 nM and the knockdown of survivin reduced survivin expression in cancer cells (A549) ( c ). The pharmacological or genetic inhibition of survivin sensitized cancer cells (A549) to chemotherapeutic reagents (GEM, gemcitabine, 0.1 µM; OSI, osimertinib, 2 µM) ( d ). * p < 0.05.

    Journal: Cancers

    Article Title: Spironolactone, a Classic Potassium-Sparing Diuretic, Reduces Survivin Expression and Chemosensitizes Cancer Cells to Non-DNA-Damaging Anticancer Drugs

    doi: 10.3390/cancers11101550

    Figure Lengend Snippet: Spironolactone decreases survivin expression and survivin reductions imitate the chemosensitizing effects of spironolactone. Cells treated with or without 25 µM spironolactone (SPL) for three days were subjected to an immunoblot analysis for survivin expression ( a , b ). YM155, a pharmacological survivin inhibitor, at the concentration of 10 nM and the knockdown of survivin reduced survivin expression in cancer cells (A549) ( c ). The pharmacological or genetic inhibition of survivin sensitized cancer cells (A549) to chemotherapeutic reagents (GEM, gemcitabine, 0.1 µM; OSI, osimertinib, 2 µM) ( d ). * p < 0.05.

    Article Snippet: The human non-small cell lung cancer (NSCLC) cell lines A549 and PC-9 were obtained from the Riken BioResource Center (Tsukuba, Japan).

    Techniques: Expressing, Western Blot, Concentration Assay, Knockdown, Inhibition

    Spironolactone induces similar effects in GS-Y01, a glioma stem cell line, to those in cancer stem cells (CSCs) of Non-small cell lung cancer (NSCLC) and pancreatic cancer. GS-Y01 cells were treated without (as control) or with the indicated concentrations of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panel) as well as the percentage of dead cells (right panel) were then assessed ( a ). Cells treated with or without spironolactone (SPL) for three days were subjected to an immunoblot analysis for survivin expression ( b ). Glioma stem cells were treated with the indicated chemotherapeutic reagents (OSI, osimertinib) in the absence or presence of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panel) as well as the percentage of dead cells (right panel) were then assessed ( c ). Values in the graphs represent the means ± SD of triplicate samples of a representative experiment repeated with similar results. * p < 0.05.

    Journal: Cancers

    Article Title: Spironolactone, a Classic Potassium-Sparing Diuretic, Reduces Survivin Expression and Chemosensitizes Cancer Cells to Non-DNA-Damaging Anticancer Drugs

    doi: 10.3390/cancers11101550

    Figure Lengend Snippet: Spironolactone induces similar effects in GS-Y01, a glioma stem cell line, to those in cancer stem cells (CSCs) of Non-small cell lung cancer (NSCLC) and pancreatic cancer. GS-Y01 cells were treated without (as control) or with the indicated concentrations of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panel) as well as the percentage of dead cells (right panel) were then assessed ( a ). Cells treated with or without spironolactone (SPL) for three days were subjected to an immunoblot analysis for survivin expression ( b ). Glioma stem cells were treated with the indicated chemotherapeutic reagents (OSI, osimertinib) in the absence or presence of spironolactone (SPL) for three days, and the numbers of viable and dead cells (left panel) as well as the percentage of dead cells (right panel) were then assessed ( c ). Values in the graphs represent the means ± SD of triplicate samples of a representative experiment repeated with similar results. * p < 0.05.

    Article Snippet: The human non-small cell lung cancer (NSCLC) cell lines A549 and PC-9 were obtained from the Riken BioResource Center (Tsukuba, Japan).

    Techniques: Control, Western Blot, Expressing

    Spironolactone sensitizes cancer cells to osimertinib in vivo. Mice (five for each group) were subcutaneously implanted with A549 cells. After the confirmation of tumor formation, mice were treated with or without osimertinib and/or spironolactone as detailed in the Materials and Methods. Tumor volume ( a ) and mouse body weight ( b ) were measured, and the results obtained are presented in the graphs as the means ± SD of each group. * p < 0.05, compared with control group in ( a ) and comparison between spironolactone treatment group and combination group in ( b ).

    Journal: Cancers

    Article Title: Spironolactone, a Classic Potassium-Sparing Diuretic, Reduces Survivin Expression and Chemosensitizes Cancer Cells to Non-DNA-Damaging Anticancer Drugs

    doi: 10.3390/cancers11101550

    Figure Lengend Snippet: Spironolactone sensitizes cancer cells to osimertinib in vivo. Mice (five for each group) were subcutaneously implanted with A549 cells. After the confirmation of tumor formation, mice were treated with or without osimertinib and/or spironolactone as detailed in the Materials and Methods. Tumor volume ( a ) and mouse body weight ( b ) were measured, and the results obtained are presented in the graphs as the means ± SD of each group. * p < 0.05, compared with control group in ( a ) and comparison between spironolactone treatment group and combination group in ( b ).

    Article Snippet: The human non-small cell lung cancer (NSCLC) cell lines A549 and PC-9 were obtained from the Riken BioResource Center (Tsukuba, Japan).

    Techniques: In Vivo, Control, Comparison