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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 pc 9 lung adenocarcinoma cell line
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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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Screening for Lm-γ2 and Lm-γ2F in serum-free conditioned media (SF-CM) from non–small-cell lung carcinoma <t>(NSCLC)</t> cells. A: Schematic representation of Lm-γ2 and Lm-γ2F proteins, including the epitopes recognized by the anti–Lm-γ2 monoclonal antibodies (mAbs) D4B5 and 23B1. B: Western blot of Lm-γ2 and its related chains. Concentrated conditioned media (100×) from NSCLC and SKOV-3 cells were subjected to Western blot analysis using mAbs 23B1 and D4B5 (NSCLC: 10 μL; SKOV-3: 2 μL). CBB, Coomassie Brilliant Blue R-250.
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Immunohistochemical staining for ARID1A expression in EGFR-mutant <t>LUAD</t> tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.
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Immunohistochemical staining for ARID1A expression in EGFR-mutant <t>LUAD</t> tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.
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Immunohistochemical staining for ARID1A expression in EGFR-mutant <t>LUAD</t> tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.
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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

Screening for Lm-γ2 and Lm-γ2F in serum-free conditioned media (SF-CM) from non–small-cell lung carcinoma (NSCLC) cells. A: Schematic representation of Lm-γ2 and Lm-γ2F proteins, including the epitopes recognized by the anti–Lm-γ2 monoclonal antibodies (mAbs) D4B5 and 23B1. B: Western blot of Lm-γ2 and its related chains. Concentrated conditioned media (100×) from NSCLC and SKOV-3 cells were subjected to Western blot analysis using mAbs 23B1 and D4B5 (NSCLC: 10 μL; SKOV-3: 2 μL). CBB, Coomassie Brilliant Blue R-250.

Journal: The American Journal of Pathology

Article Title: Laminin-γ2–NR6A1 Fusion Protein Promotes Metastatic Potential in Non–Small-Cell Lung Carcinoma Cells without Epidermal Growth Factor Receptor Mutation

doi: 10.1016/j.ajpath.2025.03.006

Figure Lengend Snippet: Screening for Lm-γ2 and Lm-γ2F in serum-free conditioned media (SF-CM) from non–small-cell lung carcinoma (NSCLC) cells. A: Schematic representation of Lm-γ2 and Lm-γ2F proteins, including the epitopes recognized by the anti–Lm-γ2 monoclonal antibodies (mAbs) D4B5 and 23B1. B: Western blot of Lm-γ2 and its related chains. Concentrated conditioned media (100×) from NSCLC and SKOV-3 cells were subjected to Western blot analysis using mAbs 23B1 and D4B5 (NSCLC: 10 μL; SKOV-3: 2 μL). CBB, Coomassie Brilliant Blue R-250.

Article Snippet: The NSCLC cell lines PC-9, NCI-H1650, NCI-H1975, EKVX, RERF-LC-KJ, and VMRC-LCD were obtained from the Japanese Collection of Research Bioresource Cell Bank (National Institute of Biomedical Innovation, Health and Nutrition, Osaka, Japan).

Techniques: Bioprocessing, Western Blot

Lm-γ2F expression promotes cell proliferation and survival through epidermal growth factor receptor (EGFR) signaling pathway. A: Western blot analysis of EGFR protein in non–small-cell lung carcinoma (NSCLC) cells. B: Western blot analysis of enforced Lm-γ2F expression in NSCLC cells using anti–Lm-γ2 (D4B5), anti–Lm-γ2F (23B1), and anti-V5 monoclonal antibodies. EKVX and RERF-LC-KJ cells expressed wild-type EGFR, whereas VMRC-LCD cells did not. C – E: Effect of enforced Lm-γ2F expression on cell proliferation in NSCLC cells (EKVX, RERF-LC-KJ, and VMRC-LCD) under two-dimensional (2-D) culture conditions with 10% fetal calf serum (FCS). Cell counts were performed using Trypan blue staining after 3, 5, and 7 days of incubation. F and G: Effect of gefitinib on NSCLC cell proliferation. Control and Lm-γ2F–expressing cells were cultured in 6-well plates with or without gefitinib under 2-D culture conditions with 10% FCS (EKVX: 500 nmol/L; RERF-LC-KJ: 250 nmol/L). Cell counts were performed using Trypan blue staining after 5 days of incubation. H and I: Effect of enforced Lm-γ2F expression on cell proliferation in NSCLC cells (EKVX and RERF-LC-KJ) under three-dimensional collagen gel culture conditions with 10% and 20% FCS, respectively. J and K: Effect of enforced Lm-γ2F expression on spheroid growth in NSCLC cells (EKVX and RERF-LC-KJ) under poly-HEMA–coated plate conditions with 10% FCS. Spheroid formation ability was quantified using ImageJ software version 1.54g. All experiments were performed in duplicate, and three independent experiments were conducted. Bar graphs represent data of at least three replicates. Statistical analysis was performed using one-way analysis of variance with Dunnett multiple comparisons test or Tukey multiple comparisons test. Data are given as means ± SD ( C – K ). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001; † P < 0.05, ††† P < 0.001. Scale bars = 100 μm ( J and K ). NS, not significant.

Journal: The American Journal of Pathology

Article Title: Laminin-γ2–NR6A1 Fusion Protein Promotes Metastatic Potential in Non–Small-Cell Lung Carcinoma Cells without Epidermal Growth Factor Receptor Mutation

doi: 10.1016/j.ajpath.2025.03.006

Figure Lengend Snippet: Lm-γ2F expression promotes cell proliferation and survival through epidermal growth factor receptor (EGFR) signaling pathway. A: Western blot analysis of EGFR protein in non–small-cell lung carcinoma (NSCLC) cells. B: Western blot analysis of enforced Lm-γ2F expression in NSCLC cells using anti–Lm-γ2 (D4B5), anti–Lm-γ2F (23B1), and anti-V5 monoclonal antibodies. EKVX and RERF-LC-KJ cells expressed wild-type EGFR, whereas VMRC-LCD cells did not. C – E: Effect of enforced Lm-γ2F expression on cell proliferation in NSCLC cells (EKVX, RERF-LC-KJ, and VMRC-LCD) under two-dimensional (2-D) culture conditions with 10% fetal calf serum (FCS). Cell counts were performed using Trypan blue staining after 3, 5, and 7 days of incubation. F and G: Effect of gefitinib on NSCLC cell proliferation. Control and Lm-γ2F–expressing cells were cultured in 6-well plates with or without gefitinib under 2-D culture conditions with 10% FCS (EKVX: 500 nmol/L; RERF-LC-KJ: 250 nmol/L). Cell counts were performed using Trypan blue staining after 5 days of incubation. H and I: Effect of enforced Lm-γ2F expression on cell proliferation in NSCLC cells (EKVX and RERF-LC-KJ) under three-dimensional collagen gel culture conditions with 10% and 20% FCS, respectively. J and K: Effect of enforced Lm-γ2F expression on spheroid growth in NSCLC cells (EKVX and RERF-LC-KJ) under poly-HEMA–coated plate conditions with 10% FCS. Spheroid formation ability was quantified using ImageJ software version 1.54g. All experiments were performed in duplicate, and three independent experiments were conducted. Bar graphs represent data of at least three replicates. Statistical analysis was performed using one-way analysis of variance with Dunnett multiple comparisons test or Tukey multiple comparisons test. Data are given as means ± SD ( C – K ). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001; † P < 0.05, ††† P < 0.001. Scale bars = 100 μm ( J and K ). NS, not significant.

Article Snippet: The NSCLC cell lines PC-9, NCI-H1650, NCI-H1975, EKVX, RERF-LC-KJ, and VMRC-LCD were obtained from the Japanese Collection of Research Bioresource Cell Bank (National Institute of Biomedical Innovation, Health and Nutrition, Osaka, Japan).

Techniques: Expressing, Western Blot, Bioprocessing, Staining, Incubation, Control, Cell Culture, Software

Summary of Lm-γ2F–induced malignant progression in non–small-cell lung carcinoma (NSCLC) without epidermal growth factor receptor (EGFR) mutations. A: Ectopic expression of Lm-γ2F activates EGFR and its downstream signaling pathways, including AKT and extracellular signal-regulated kinase (ERK), in NSCLC cells lacking EGFR mutations. B: This activation promotes cell proliferation, motility, survival, invasion, and metastasis. EGFR tyrosine kinase inhibitors are suggested to inhibit the acquisition of malignant traits in patients with NSCLC without EGFR mutations expressing Lm-γ2F.

Journal: The American Journal of Pathology

Article Title: Laminin-γ2–NR6A1 Fusion Protein Promotes Metastatic Potential in Non–Small-Cell Lung Carcinoma Cells without Epidermal Growth Factor Receptor Mutation

doi: 10.1016/j.ajpath.2025.03.006

Figure Lengend Snippet: Summary of Lm-γ2F–induced malignant progression in non–small-cell lung carcinoma (NSCLC) without epidermal growth factor receptor (EGFR) mutations. A: Ectopic expression of Lm-γ2F activates EGFR and its downstream signaling pathways, including AKT and extracellular signal-regulated kinase (ERK), in NSCLC cells lacking EGFR mutations. B: This activation promotes cell proliferation, motility, survival, invasion, and metastasis. EGFR tyrosine kinase inhibitors are suggested to inhibit the acquisition of malignant traits in patients with NSCLC without EGFR mutations expressing Lm-γ2F.

Article Snippet: The NSCLC cell lines PC-9, NCI-H1650, NCI-H1975, EKVX, RERF-LC-KJ, and VMRC-LCD were obtained from the Japanese Collection of Research Bioresource Cell Bank (National Institute of Biomedical Innovation, Health and Nutrition, Osaka, Japan).

Techniques: Expressing, Protein-Protein interactions, Activation Assay

Immunohistochemical staining for ARID1A expression in EGFR-mutant LUAD tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: Immunohistochemical staining for ARID1A expression in EGFR-mutant LUAD tissues (50×and 200×). (A) ARID1A low expression. (B) ARID1A high expression.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Immunohistochemical staining, Staining, Expressing, Mutagenesis

SWI/SNF subunit mutations in lung adenocarcinoma (LUAD). (A) The frequencies of EGFR and SWI/SNF subunit mutations in LUAD. (B) The frequency of SWI/SNF subunit mutations in EGFR-mutant LUAD. (C) The types of SWI/SNF subunit mutations in EGFR-mutant LUAD.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: SWI/SNF subunit mutations in lung adenocarcinoma (LUAD). (A) The frequencies of EGFR and SWI/SNF subunit mutations in LUAD. (B) The frequency of SWI/SNF subunit mutations in EGFR-mutant LUAD. (C) The types of SWI/SNF subunit mutations in EGFR-mutant LUAD.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Mutagenesis

The role of SWI/SNF subunit mutations in the prognosis of EGFR-mutant LUAD. (A-F) ARID1A, ARID1B, ARID2, ARID5B, SMARCA4, and SMARCB1.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of SWI/SNF subunit mutations in the prognosis of EGFR-mutant LUAD. (A-F) ARID1A, ARID1B, ARID2, ARID5B, SMARCA4, and SMARCB1.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Mutagenesis

ARID1A mutation confers a poor prognosis for patients with EGFR-mutant LUAD. (A) The frequencies of genes exhibiting coexisting mutations with EGFR. Survival analysis for patients with the EGFR mutation, ARID1A/EGFR comutation and (B) TP53/EGFR, (C) KRAS/EGFR, (D) CDKN2A/EGFR, (E) PIK3CA/EGFR, (F) RB1/EGFR, and (G) PTEN/EGFR comutations.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: ARID1A mutation confers a poor prognosis for patients with EGFR-mutant LUAD. (A) The frequencies of genes exhibiting coexisting mutations with EGFR. Survival analysis for patients with the EGFR mutation, ARID1A/EGFR comutation and (B) TP53/EGFR, (C) KRAS/EGFR, (D) CDKN2A/EGFR, (E) PIK3CA/EGFR, (F) RB1/EGFR, and (G) PTEN/EGFR comutations.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Mutagenesis

The role of ARID1A expression in the prognosis of EGFR-mutant LUAD patients receiving EGFR-TKIs as a first-line treatment after postoperative progression. (A) Comparison of PFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for the univariate and multivariate analyses of PFS.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of ARID1A expression in the prognosis of EGFR-mutant LUAD patients receiving EGFR-TKIs as a first-line treatment after postoperative progression. (A) Comparison of PFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for the univariate and multivariate analyses of PFS.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Expressing, Mutagenesis, Comparison

The role of ARID1A in the prognosis of EGFR-mutant LUAD patients receiving postoperative adjuvant EGFR-TKI treatments. (A) Comparison of DFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for univariate and multivariate analyses of DFS. (C) Nomogram for the prediction of 1-, 2- and 3-year survival. (D) Calibration curves of the nomogram.

Journal: Frontiers in Pharmacology

Article Title: ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma

doi: 10.3389/fphar.2025.1582005

Figure Lengend Snippet: The role of ARID1A in the prognosis of EGFR-mutant LUAD patients receiving postoperative adjuvant EGFR-TKI treatments. (A) Comparison of DFS between patients with low ARID1A expression and patients with high ARID1A expression. (B) Forest plots for univariate and multivariate analyses of DFS. (C) Nomogram for the prediction of 1-, 2- and 3-year survival. (D) Calibration curves of the nomogram.

Article Snippet: LUAD cell line PC-9 (Procell Life Science, Wuhan, China) was maintained in RPMI-1640 medium supplemented with 10% FBS under standard humidified conditions (37°C, 5% CO 2 ).

Techniques: Mutagenesis, Adjuvant, Comparison, Expressing