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human small cell lung cancer sclc cell lines h69  (ATCC)


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    ATCC human small cell lung cancer sclc cell lines h69
    Dose- and time-dependent suppression of <t>SCLC</t> cell proliferation and clonogenicity by Chidamide. A–C Dose–response curves of <t>H69,</t> H526, and H446 cells treated with Chidamide at various concentrations for 24–96 h, assessed by CCK-8 assay. D Representative images of clonogenic assays 48 h after treatment with Chidamide at IC10, IC20, and IC50 concentrations (Scale bar: 626.1 μm). E–G Quantitative analysis of colony numbers from three independent experiments, and one-way ANOVA followed by Dunnett’s post hoc test was performed (mean ± SD, n = 3 independent experiments; ** P < 0.01, *** P < 0.001)
    Human Small Cell Lung Cancer Sclc Cell Lines H69, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1983 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human small cell lung cancer sclc cell lines h69/product/ATCC
    Average 96 stars, based on 1983 article reviews
    human small cell lung cancer sclc cell lines h69 - by Bioz Stars, 2026-03
    96/100 stars

    Images

    1) Product Images from "Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes"

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    Journal: Discover Oncology

    doi: 10.1007/s12672-025-04356-4

    Dose- and time-dependent suppression of SCLC cell proliferation and clonogenicity by Chidamide. A–C Dose–response curves of H69, H526, and H446 cells treated with Chidamide at various concentrations for 24–96 h, assessed by CCK-8 assay. D Representative images of clonogenic assays 48 h after treatment with Chidamide at IC10, IC20, and IC50 concentrations (Scale bar: 626.1 μm). E–G Quantitative analysis of colony numbers from three independent experiments, and one-way ANOVA followed by Dunnett’s post hoc test was performed (mean ± SD, n = 3 independent experiments; ** P < 0.01, *** P < 0.001)
    Figure Legend Snippet: Dose- and time-dependent suppression of SCLC cell proliferation and clonogenicity by Chidamide. A–C Dose–response curves of H69, H526, and H446 cells treated with Chidamide at various concentrations for 24–96 h, assessed by CCK-8 assay. D Representative images of clonogenic assays 48 h after treatment with Chidamide at IC10, IC20, and IC50 concentrations (Scale bar: 626.1 μm). E–G Quantitative analysis of colony numbers from three independent experiments, and one-way ANOVA followed by Dunnett’s post hoc test was performed (mean ± SD, n = 3 independent experiments; ** P < 0.01, *** P < 0.001)

    Techniques Used: CCK-8 Assay

    Dose-dependent apoptosis induction and G1-phase arrest in Chidamide-treated SCLC cells. A Apoptosis analysis by flow cytometry: Representative Annexin V-FITC/PI dot plots (left) and quantified apoptotic rates (histogram, right) of H69, H526, and H446 cells treated with 0.1% DMSO (Control) and Chidamide at IC 10 , IC 20 , and IC 50 concentrations (H69: 0.163, 0.572, 4.9 μM; H526: 0.278, 0.566, 1.979 μM; H446: 0.122, 0.347, 2.073 μM) for 48 h. B Cell cycle analysis: DNA content histograms (left) and quantified G1/S/G2 phase distributions (histogram, right) of cells treated as in A . Data (mean ± SD, n = 3 independent experiments) were analyzed using GraphPad Prism 5 software. Comparisons with the control group were performed using one-way ANOVA and two-way ANOVA followed by Dunnett’s post-hoc test (*** P < 0.001, ns )
    Figure Legend Snippet: Dose-dependent apoptosis induction and G1-phase arrest in Chidamide-treated SCLC cells. A Apoptosis analysis by flow cytometry: Representative Annexin V-FITC/PI dot plots (left) and quantified apoptotic rates (histogram, right) of H69, H526, and H446 cells treated with 0.1% DMSO (Control) and Chidamide at IC 10 , IC 20 , and IC 50 concentrations (H69: 0.163, 0.572, 4.9 μM; H526: 0.278, 0.566, 1.979 μM; H446: 0.122, 0.347, 2.073 μM) for 48 h. B Cell cycle analysis: DNA content histograms (left) and quantified G1/S/G2 phase distributions (histogram, right) of cells treated as in A . Data (mean ± SD, n = 3 independent experiments) were analyzed using GraphPad Prism 5 software. Comparisons with the control group were performed using one-way ANOVA and two-way ANOVA followed by Dunnett’s post-hoc test (*** P < 0.001, ns )

    Techniques Used: Flow Cytometry, Control, Cell Cycle Assay, Software

    Chidamide alters histone acetylation, cell cycle regulators, and mitochondrial apoptosis in SCLC cells. ( A, D, G ) H69, ( B, E, H ) H526, and ( C, F, I ) H446 cells were treated with Chidamide at indicated concentrations or DMSO control for 48 h. Western blot analysis demonstrated dose-dependent decrease in HDAC1/2/3, increase in Ac-H3 and Ac-H4, downregulation of Cyclin E1 and CDK2, upregulation of p21 and p27, and activation of mitochondrial apoptosis via altered Bcl-2 and Bax expression. GAPDH was used as loading control. Data represent three independent experiments
    Figure Legend Snippet: Chidamide alters histone acetylation, cell cycle regulators, and mitochondrial apoptosis in SCLC cells. ( A, D, G ) H69, ( B, E, H ) H526, and ( C, F, I ) H446 cells were treated with Chidamide at indicated concentrations or DMSO control for 48 h. Western blot analysis demonstrated dose-dependent decrease in HDAC1/2/3, increase in Ac-H3 and Ac-H4, downregulation of Cyclin E1 and CDK2, upregulation of p21 and p27, and activation of mitochondrial apoptosis via altered Bcl-2 and Bax expression. GAPDH was used as loading control. Data represent three independent experiments

    Techniques Used: Control, Western Blot, Activation Assay, Expressing

    Potent dose-dependent antitumor activity of chidamide with no overt signs of toxicity in SCLC xenografts ( A ) Representative images of subcutaneous tumors derived from H69, H526, and H446 cells in nude mice treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide for 21 days. B–D Tumor volume dynamics in H69, H526, and H446 xenografts, showing significant growth inhibition in Chidamide-treated groups compared to Control. (E–G) Body weight monitoring revealed no significant differences among groups. Data are mean ± SD (n = 3 mice/group); color-coded lines: orange (Control), green (Low Dose), and blue (High Dose). Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (** P < 0.01, *** P < 0.001, ns )
    Figure Legend Snippet: Potent dose-dependent antitumor activity of chidamide with no overt signs of toxicity in SCLC xenografts ( A ) Representative images of subcutaneous tumors derived from H69, H526, and H446 cells in nude mice treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide for 21 days. B–D Tumor volume dynamics in H69, H526, and H446 xenografts, showing significant growth inhibition in Chidamide-treated groups compared to Control. (E–G) Body weight monitoring revealed no significant differences among groups. Data are mean ± SD (n = 3 mice/group); color-coded lines: orange (Control), green (Low Dose), and blue (High Dose). Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (** P < 0.01, *** P < 0.001, ns )

    Techniques Used: Activity Assay, Derivative Assay, Control, Inhibition

    Chidamide promotes apoptosis and necrosis in SCLC xenograft models: H&E and TUNEL analyses. A Representative hematoxylin and eosin (H&E)-stained sections of H69, H526, and H446 xenografts treated with vehicle (Control), low dose (12.5 mg/kg), and high dose (25 mg/kg) Chidamide. Histopathological analysis reveals increased necrotic areas (pink eosinophilic zones) and reduced viable tumor cells in high-dose groups (Scale bar: 60 μm). B–D TUNEL staining (green) combined with DAPI nuclear counterstaining (blue) in H69 ( B ), H526 ( C ), and H446 ( D ) xenografts. Apoptotic cells (TUNEL + /DAPI +) exhibit dose-dependent enrichment, with the highest apoptotic rate in high-dose groups (Scale bar: 50 μm). E–G Quantitative analysis of TUNEL fluorescence intensity in H69 ( E ), H526 ( F ), and H446 ( G ) tumors. Statistical analysis was performed using GraphPad Prism 5 with one-way ANOVA followed by Dunnett’s post-hoc test for comparisons against the control group (mean ± SD, n = 3 biological replicates; * P < 0.05, ** P < 0.01, *** P < 0.001)
    Figure Legend Snippet: Chidamide promotes apoptosis and necrosis in SCLC xenograft models: H&E and TUNEL analyses. A Representative hematoxylin and eosin (H&E)-stained sections of H69, H526, and H446 xenografts treated with vehicle (Control), low dose (12.5 mg/kg), and high dose (25 mg/kg) Chidamide. Histopathological analysis reveals increased necrotic areas (pink eosinophilic zones) and reduced viable tumor cells in high-dose groups (Scale bar: 60 μm). B–D TUNEL staining (green) combined with DAPI nuclear counterstaining (blue) in H69 ( B ), H526 ( C ), and H446 ( D ) xenografts. Apoptotic cells (TUNEL + /DAPI +) exhibit dose-dependent enrichment, with the highest apoptotic rate in high-dose groups (Scale bar: 50 μm). E–G Quantitative analysis of TUNEL fluorescence intensity in H69 ( E ), H526 ( F ), and H446 ( G ) tumors. Statistical analysis was performed using GraphPad Prism 5 with one-way ANOVA followed by Dunnett’s post-hoc test for comparisons against the control group (mean ± SD, n = 3 biological replicates; * P < 0.05, ** P < 0.01, *** P < 0.001)

    Techniques Used: TUNEL Assay, Staining, Control, Fluorescence

    Immunohistochemical and Western blot analyses of histone acetylation, DNA damage markers, and apoptosis-related proteins in Chidamide-treated SCLC xenografts. A–C Immunohistochemical (IHC) staining of formalin-fixed paraffin-embedded tumor sections from H69, H526, and H446 xenografts treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide, assessing Ac-H3, γ-H2AX, p21, and Cleaved caspase-3 expression (Scale bar: 20 μm). D–F Quantification of IHC staining intensity (mean optical density ± SD, n = 3 independent experiments) using Image-Pro Plus software. G Western blot analysis of tumor lysates for H3, Ac-H3, γ-H2AX, p21, Caspase-3, and Cleaved caspase-3. GAPDH served as a loading control. Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (* P < 0.05, ** P < 0.01, *** P < 0.001, ns )
    Figure Legend Snippet: Immunohistochemical and Western blot analyses of histone acetylation, DNA damage markers, and apoptosis-related proteins in Chidamide-treated SCLC xenografts. A–C Immunohistochemical (IHC) staining of formalin-fixed paraffin-embedded tumor sections from H69, H526, and H446 xenografts treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide, assessing Ac-H3, γ-H2AX, p21, and Cleaved caspase-3 expression (Scale bar: 20 μm). D–F Quantification of IHC staining intensity (mean optical density ± SD, n = 3 independent experiments) using Image-Pro Plus software. G Western blot analysis of tumor lysates for H3, Ac-H3, γ-H2AX, p21, Caspase-3, and Cleaved caspase-3. GAPDH served as a loading control. Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (* P < 0.05, ** P < 0.01, *** P < 0.001, ns )

    Techniques Used: Immunohistochemical staining, Western Blot, Immunohistochemistry, Formalin-fixed Paraffin-Embedded, Control, Expressing, Software



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    Dose- and time-dependent suppression of SCLC cell proliferation and clonogenicity by Chidamide. A–C Dose–response curves of H69, H526, and H446 cells treated with Chidamide at various concentrations for 24–96 h, assessed by CCK-8 assay. D Representative images of clonogenic assays 48 h after treatment with Chidamide at IC10, IC20, and IC50 concentrations (Scale bar: 626.1 μm). E–G Quantitative analysis of colony numbers from three independent experiments, and one-way ANOVA followed by Dunnett’s post hoc test was performed (mean ± SD, n = 3 independent experiments; ** P < 0.01, *** P < 0.001)

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Dose- and time-dependent suppression of SCLC cell proliferation and clonogenicity by Chidamide. A–C Dose–response curves of H69, H526, and H446 cells treated with Chidamide at various concentrations for 24–96 h, assessed by CCK-8 assay. D Representative images of clonogenic assays 48 h after treatment with Chidamide at IC10, IC20, and IC50 concentrations (Scale bar: 626.1 μm). E–G Quantitative analysis of colony numbers from three independent experiments, and one-way ANOVA followed by Dunnett’s post hoc test was performed (mean ± SD, n = 3 independent experiments; ** P < 0.01, *** P < 0.001)

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: CCK-8 Assay

    Dose-dependent apoptosis induction and G1-phase arrest in Chidamide-treated SCLC cells. A Apoptosis analysis by flow cytometry: Representative Annexin V-FITC/PI dot plots (left) and quantified apoptotic rates (histogram, right) of H69, H526, and H446 cells treated with 0.1% DMSO (Control) and Chidamide at IC 10 , IC 20 , and IC 50 concentrations (H69: 0.163, 0.572, 4.9 μM; H526: 0.278, 0.566, 1.979 μM; H446: 0.122, 0.347, 2.073 μM) for 48 h. B Cell cycle analysis: DNA content histograms (left) and quantified G1/S/G2 phase distributions (histogram, right) of cells treated as in A . Data (mean ± SD, n = 3 independent experiments) were analyzed using GraphPad Prism 5 software. Comparisons with the control group were performed using one-way ANOVA and two-way ANOVA followed by Dunnett’s post-hoc test (*** P < 0.001, ns )

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Dose-dependent apoptosis induction and G1-phase arrest in Chidamide-treated SCLC cells. A Apoptosis analysis by flow cytometry: Representative Annexin V-FITC/PI dot plots (left) and quantified apoptotic rates (histogram, right) of H69, H526, and H446 cells treated with 0.1% DMSO (Control) and Chidamide at IC 10 , IC 20 , and IC 50 concentrations (H69: 0.163, 0.572, 4.9 μM; H526: 0.278, 0.566, 1.979 μM; H446: 0.122, 0.347, 2.073 μM) for 48 h. B Cell cycle analysis: DNA content histograms (left) and quantified G1/S/G2 phase distributions (histogram, right) of cells treated as in A . Data (mean ± SD, n = 3 independent experiments) were analyzed using GraphPad Prism 5 software. Comparisons with the control group were performed using one-way ANOVA and two-way ANOVA followed by Dunnett’s post-hoc test (*** P < 0.001, ns )

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: Flow Cytometry, Control, Cell Cycle Assay, Software

    Chidamide alters histone acetylation, cell cycle regulators, and mitochondrial apoptosis in SCLC cells. ( A, D, G ) H69, ( B, E, H ) H526, and ( C, F, I ) H446 cells were treated with Chidamide at indicated concentrations or DMSO control for 48 h. Western blot analysis demonstrated dose-dependent decrease in HDAC1/2/3, increase in Ac-H3 and Ac-H4, downregulation of Cyclin E1 and CDK2, upregulation of p21 and p27, and activation of mitochondrial apoptosis via altered Bcl-2 and Bax expression. GAPDH was used as loading control. Data represent three independent experiments

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Chidamide alters histone acetylation, cell cycle regulators, and mitochondrial apoptosis in SCLC cells. ( A, D, G ) H69, ( B, E, H ) H526, and ( C, F, I ) H446 cells were treated with Chidamide at indicated concentrations or DMSO control for 48 h. Western blot analysis demonstrated dose-dependent decrease in HDAC1/2/3, increase in Ac-H3 and Ac-H4, downregulation of Cyclin E1 and CDK2, upregulation of p21 and p27, and activation of mitochondrial apoptosis via altered Bcl-2 and Bax expression. GAPDH was used as loading control. Data represent three independent experiments

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: Control, Western Blot, Activation Assay, Expressing

    Potent dose-dependent antitumor activity of chidamide with no overt signs of toxicity in SCLC xenografts ( A ) Representative images of subcutaneous tumors derived from H69, H526, and H446 cells in nude mice treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide for 21 days. B–D Tumor volume dynamics in H69, H526, and H446 xenografts, showing significant growth inhibition in Chidamide-treated groups compared to Control. (E–G) Body weight monitoring revealed no significant differences among groups. Data are mean ± SD (n = 3 mice/group); color-coded lines: orange (Control), green (Low Dose), and blue (High Dose). Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (** P < 0.01, *** P < 0.001, ns )

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Potent dose-dependent antitumor activity of chidamide with no overt signs of toxicity in SCLC xenografts ( A ) Representative images of subcutaneous tumors derived from H69, H526, and H446 cells in nude mice treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide for 21 days. B–D Tumor volume dynamics in H69, H526, and H446 xenografts, showing significant growth inhibition in Chidamide-treated groups compared to Control. (E–G) Body weight monitoring revealed no significant differences among groups. Data are mean ± SD (n = 3 mice/group); color-coded lines: orange (Control), green (Low Dose), and blue (High Dose). Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (** P < 0.01, *** P < 0.001, ns )

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: Activity Assay, Derivative Assay, Control, Inhibition

    Chidamide promotes apoptosis and necrosis in SCLC xenograft models: H&E and TUNEL analyses. A Representative hematoxylin and eosin (H&E)-stained sections of H69, H526, and H446 xenografts treated with vehicle (Control), low dose (12.5 mg/kg), and high dose (25 mg/kg) Chidamide. Histopathological analysis reveals increased necrotic areas (pink eosinophilic zones) and reduced viable tumor cells in high-dose groups (Scale bar: 60 μm). B–D TUNEL staining (green) combined with DAPI nuclear counterstaining (blue) in H69 ( B ), H526 ( C ), and H446 ( D ) xenografts. Apoptotic cells (TUNEL + /DAPI +) exhibit dose-dependent enrichment, with the highest apoptotic rate in high-dose groups (Scale bar: 50 μm). E–G Quantitative analysis of TUNEL fluorescence intensity in H69 ( E ), H526 ( F ), and H446 ( G ) tumors. Statistical analysis was performed using GraphPad Prism 5 with one-way ANOVA followed by Dunnett’s post-hoc test for comparisons against the control group (mean ± SD, n = 3 biological replicates; * P < 0.05, ** P < 0.01, *** P < 0.001)

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Chidamide promotes apoptosis and necrosis in SCLC xenograft models: H&E and TUNEL analyses. A Representative hematoxylin and eosin (H&E)-stained sections of H69, H526, and H446 xenografts treated with vehicle (Control), low dose (12.5 mg/kg), and high dose (25 mg/kg) Chidamide. Histopathological analysis reveals increased necrotic areas (pink eosinophilic zones) and reduced viable tumor cells in high-dose groups (Scale bar: 60 μm). B–D TUNEL staining (green) combined with DAPI nuclear counterstaining (blue) in H69 ( B ), H526 ( C ), and H446 ( D ) xenografts. Apoptotic cells (TUNEL + /DAPI +) exhibit dose-dependent enrichment, with the highest apoptotic rate in high-dose groups (Scale bar: 50 μm). E–G Quantitative analysis of TUNEL fluorescence intensity in H69 ( E ), H526 ( F ), and H446 ( G ) tumors. Statistical analysis was performed using GraphPad Prism 5 with one-way ANOVA followed by Dunnett’s post-hoc test for comparisons against the control group (mean ± SD, n = 3 biological replicates; * P < 0.05, ** P < 0.01, *** P < 0.001)

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: TUNEL Assay, Staining, Control, Fluorescence

    Immunohistochemical and Western blot analyses of histone acetylation, DNA damage markers, and apoptosis-related proteins in Chidamide-treated SCLC xenografts. A–C Immunohistochemical (IHC) staining of formalin-fixed paraffin-embedded tumor sections from H69, H526, and H446 xenografts treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide, assessing Ac-H3, γ-H2AX, p21, and Cleaved caspase-3 expression (Scale bar: 20 μm). D–F Quantification of IHC staining intensity (mean optical density ± SD, n = 3 independent experiments) using Image-Pro Plus software. G Western blot analysis of tumor lysates for H3, Ac-H3, γ-H2AX, p21, Caspase-3, and Cleaved caspase-3. GAPDH served as a loading control. Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (* P < 0.05, ** P < 0.01, *** P < 0.001, ns )

    Journal: Discover Oncology

    Article Title: Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes

    doi: 10.1007/s12672-025-04356-4

    Figure Lengend Snippet: Immunohistochemical and Western blot analyses of histone acetylation, DNA damage markers, and apoptosis-related proteins in Chidamide-treated SCLC xenografts. A–C Immunohistochemical (IHC) staining of formalin-fixed paraffin-embedded tumor sections from H69, H526, and H446 xenografts treated with vehicle (Control), low-dose (12.5 mg/kg), and high-dose (25 mg/kg) Chidamide, assessing Ac-H3, γ-H2AX, p21, and Cleaved caspase-3 expression (Scale bar: 20 μm). D–F Quantification of IHC staining intensity (mean optical density ± SD, n = 3 independent experiments) using Image-Pro Plus software. G Western blot analysis of tumor lysates for H3, Ac-H3, γ-H2AX, p21, Caspase-3, and Cleaved caspase-3. GAPDH served as a loading control. Statistical analysis was performed using GraphPad Prism 5 with two-way ANOVA followed by the Bonferroni test (* P < 0.05, ** P < 0.01, *** P < 0.001, ns )

    Article Snippet: Human small cell lung cancer (SCLC) cell lines H69, H526, and H446 were purchased from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium (Gibco) supplemented with 10% fetal bovine serum (FBS; Gibco), 1% penicillin streptomycin, and 1.5% HEPES at 37 °C, 5% CO 2 , and 90% humidity.

    Techniques: Immunohistochemical staining, Western Blot, Immunohistochemistry, Formalin-fixed Paraffin-Embedded, Control, Expressing, Software

    DDX5 protein is more stable in SCLC (A) Representative western blot images showing the amount of DDX5, RFC1, and GAPDH proteins in HBEC-3KT, H69 and H69AR cells. (B) Bar graphs depict the quantification of DDX5, RFC1, and GAPDH protein from three different biological replicates in the form of mean ± standard deviation (SD). (C) DDX5 gene expression profile of 23 clinical small cell lung cancer (SCLC) samples from patients in comparison to normal lung tissue obtained from Gene Expression Omnibus (GEO): GDS4794/225886_at. (D) Profile of DDX5 gene expression across all tumor samples and paired normal tissues from Gene Expression Profiling Interactive Analysis (GEPIA): ENSG00000108654.11. Log 2 FC cutoff was set at 1 and the p value cutoff was set at 0.01. (E) RT-qPCR was used to quantify levels of DDX5 transcripts in HBEC-3KT, H69 and H69AR samples, which were normalized to the expression levels of GAPDH mRNA in the form of mean ± standard deviation (SD) from three biological replicates. (F–H) The stability of DDX5 and RFC1 proteins in HBEC-3KT, H69 and H69AR cells was measured by cycloheximide (CHX) chase assay. RFC1 is a positive control and GAPDH is used as a loading control. (I and J) Graphical representation of DDX5 and RFC1 protein degradation using the CHX assay. The half-lives were determined from three biological replicates and the signals were normalized to GAPDH. The p values are ∗<0.05, ∗∗<0.005, and ∗∗∗<0.001; ns, not significant.

    Journal: iScience

    Article Title: Supinoxin blocks small cell lung cancer progression by inhibiting mitochondrial respiration through DDX5

    doi: 10.1016/j.isci.2025.112219

    Figure Lengend Snippet: DDX5 protein is more stable in SCLC (A) Representative western blot images showing the amount of DDX5, RFC1, and GAPDH proteins in HBEC-3KT, H69 and H69AR cells. (B) Bar graphs depict the quantification of DDX5, RFC1, and GAPDH protein from three different biological replicates in the form of mean ± standard deviation (SD). (C) DDX5 gene expression profile of 23 clinical small cell lung cancer (SCLC) samples from patients in comparison to normal lung tissue obtained from Gene Expression Omnibus (GEO): GDS4794/225886_at. (D) Profile of DDX5 gene expression across all tumor samples and paired normal tissues from Gene Expression Profiling Interactive Analysis (GEPIA): ENSG00000108654.11. Log 2 FC cutoff was set at 1 and the p value cutoff was set at 0.01. (E) RT-qPCR was used to quantify levels of DDX5 transcripts in HBEC-3KT, H69 and H69AR samples, which were normalized to the expression levels of GAPDH mRNA in the form of mean ± standard deviation (SD) from three biological replicates. (F–H) The stability of DDX5 and RFC1 proteins in HBEC-3KT, H69 and H69AR cells was measured by cycloheximide (CHX) chase assay. RFC1 is a positive control and GAPDH is used as a loading control. (I and J) Graphical representation of DDX5 and RFC1 protein degradation using the CHX assay. The half-lives were determined from three biological replicates and the signals were normalized to GAPDH. The p values are ∗<0.05, ∗∗<0.005, and ∗∗∗<0.001; ns, not significant.

    Article Snippet: Human SCLC cell lines NCI-H69 (H69) and NCI-H69AR (H69AR) cells were purchased from American Type Culture Collection (ATCC).

    Techniques: Western Blot, Standard Deviation, Gene Expression, Comparison, Quantitative RT-PCR, Expressing, Positive Control, Control

    Dose-response curve of Supinoxin in H69 and H69AR cells (A and B) Varying concentrations of Supinoxin were tested in H69 cells (A) and H69AR cells (B) grown in a 96-well plate for 24 h, after which cell viability was measured using a CyQUANT direct cell proliferation assay Kit. IC 50 was calculated from three biological replicates. (C and D) Soft agar colony formation assays were also performed with 0 and 40 nM Supinoxin in H69 cells (C) and 0 and 70 nM Supinoxin in H69AR cells. (E and F) Quantification of H69 (E) and H69AR (F) soft agar colony assays from three biological replicates in the form of mean ± standard deviation (SD). The p values are ∗<0.05, ∗∗<0.005, and ∗∗∗<0.001; ns, not significant.

    Journal: iScience

    Article Title: Supinoxin blocks small cell lung cancer progression by inhibiting mitochondrial respiration through DDX5

    doi: 10.1016/j.isci.2025.112219

    Figure Lengend Snippet: Dose-response curve of Supinoxin in H69 and H69AR cells (A and B) Varying concentrations of Supinoxin were tested in H69 cells (A) and H69AR cells (B) grown in a 96-well plate for 24 h, after which cell viability was measured using a CyQUANT direct cell proliferation assay Kit. IC 50 was calculated from three biological replicates. (C and D) Soft agar colony formation assays were also performed with 0 and 40 nM Supinoxin in H69 cells (C) and 0 and 70 nM Supinoxin in H69AR cells. (E and F) Quantification of H69 (E) and H69AR (F) soft agar colony assays from three biological replicates in the form of mean ± standard deviation (SD). The p values are ∗<0.05, ∗∗<0.005, and ∗∗∗<0.001; ns, not significant.

    Article Snippet: Human SCLC cell lines NCI-H69 (H69) and NCI-H69AR (H69AR) cells were purchased from American Type Culture Collection (ATCC).

    Techniques: CyQUANT Assay, Proliferation Assay, Standard Deviation

    Journal: iScience

    Article Title: Supinoxin blocks small cell lung cancer progression by inhibiting mitochondrial respiration through DDX5

    doi: 10.1016/j.isci.2025.112219

    Figure Lengend Snippet:

    Article Snippet: Human SCLC cell lines NCI-H69 (H69) and NCI-H69AR (H69AR) cells were purchased from American Type Culture Collection (ATCC).

    Techniques: Recombinant, SYBR Green Assay, Lysis, Protease Inhibitor, Western Blot, Plasmid Preparation, Modification, CyQUANT Assay, Proliferation Assay, Reverse Transcription, RNA Sequencing, Gene Expression, Software

    Cell morphology of human SCLC cell lines. Representative light microscopy images showing the growth patterns and cell morphology of human SCLC cells. Scale bars: 20 μm, except for H69M (100 μm).

    Journal: International Journal of Molecular Sciences

    Article Title: The Potential of Single-Transcription Factor Gene Expression by RT-qPCR for Subtyping Small Cell Lung Cancer

    doi: 10.3390/ijms26031293

    Figure Lengend Snippet: Cell morphology of human SCLC cell lines. Representative light microscopy images showing the growth patterns and cell morphology of human SCLC cells. Scale bars: 20 μm, except for H69M (100 μm).

    Article Snippet: Human SCLC cell lines, including H69 (ATCC number: HTB-119, RRID: CVCL_1579), Shp77 (ATCC number: CRL-2195, RRID: CVCL_1693), H748 (ATCC number: CRL-5841, RRID: CVCL_1588), H345 (ATCC number: HTB-180, RRID: CVCL_1558), H82 (ATCC number: HTB-175, RRID: CVCL_1591), H1048 (ATCC number: CRL-5853, RRID: CVCL_1453), H526 (ATCC number: HTB-119, RRID: CVCL_1569), and H196 (ATCC number: HTB-119, RRID: CVCL_1509), were obtained from the American Type Culture Collection (ATCC), while the DMS273 (ECACC number: 95,062,830, RRID: CVCL_1176), cell line was obtained from the European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Light Microscopy

    Subtype classification of human SCLC cell lines. ( A ) Basal mRNA expression levels of ASCL1 , NEUROD1, and POU2F3 in human SCLC cell lines were measured as 1/ΔCt (Ct gene−Ct GAPDH ), with GAPDH as the housekeeping gene using RT-qPCR. Cells were plated and cultured for 48 h prior to RNA extraction. The plots represent the mean ± SD of three biological replicates for each cell line. ( B ) Basal protein expression analysis of ASCL1 , NEUROD1 , and POU2F3 by Western blot. Cells were plated and cultured for 48 h prior to whole protein lysate extraction. Actin was used as the housekeeping control. The images are representative of three independent biological replicates. Expected molecular weights: ASCL1 (34 kDa), NEUROD1 (40 kDa), POU2F3 (47 kDa), and GAPDH (37 kDa). The numbers and bands on the right indicate the protein ladder and the corresponding molecular weight. ( C ) Bar chart representing the quantitative densitometry analysis of basal protein expression levels of ASCL1 , NEUROD1 , and POU2F3 by Western blot. Data are presented as mean ± SD relative protein expression to housekeeping (three independent biological replicates for each cell line).

    Journal: International Journal of Molecular Sciences

    Article Title: The Potential of Single-Transcription Factor Gene Expression by RT-qPCR for Subtyping Small Cell Lung Cancer

    doi: 10.3390/ijms26031293

    Figure Lengend Snippet: Subtype classification of human SCLC cell lines. ( A ) Basal mRNA expression levels of ASCL1 , NEUROD1, and POU2F3 in human SCLC cell lines were measured as 1/ΔCt (Ct gene−Ct GAPDH ), with GAPDH as the housekeeping gene using RT-qPCR. Cells were plated and cultured for 48 h prior to RNA extraction. The plots represent the mean ± SD of three biological replicates for each cell line. ( B ) Basal protein expression analysis of ASCL1 , NEUROD1 , and POU2F3 by Western blot. Cells were plated and cultured for 48 h prior to whole protein lysate extraction. Actin was used as the housekeeping control. The images are representative of three independent biological replicates. Expected molecular weights: ASCL1 (34 kDa), NEUROD1 (40 kDa), POU2F3 (47 kDa), and GAPDH (37 kDa). The numbers and bands on the right indicate the protein ladder and the corresponding molecular weight. ( C ) Bar chart representing the quantitative densitometry analysis of basal protein expression levels of ASCL1 , NEUROD1 , and POU2F3 by Western blot. Data are presented as mean ± SD relative protein expression to housekeeping (three independent biological replicates for each cell line).

    Article Snippet: Human SCLC cell lines, including H69 (ATCC number: HTB-119, RRID: CVCL_1579), Shp77 (ATCC number: CRL-2195, RRID: CVCL_1693), H748 (ATCC number: CRL-5841, RRID: CVCL_1588), H345 (ATCC number: HTB-180, RRID: CVCL_1558), H82 (ATCC number: HTB-175, RRID: CVCL_1591), H1048 (ATCC number: CRL-5853, RRID: CVCL_1453), H526 (ATCC number: HTB-119, RRID: CVCL_1569), and H196 (ATCC number: HTB-119, RRID: CVCL_1509), were obtained from the American Type Culture Collection (ATCC), while the DMS273 (ECACC number: 95,062,830, RRID: CVCL_1176), cell line was obtained from the European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Expressing, Quantitative RT-PCR, Cell Culture, RNA Extraction, Western Blot, Extraction, Control, Molecular Weight

    Cell morphology of mouse SCLC cell lines. Representative light microscopy images showing the growth patterns and cell morphology of mouse SCLC cells. Scale bars: 20 μm.

    Journal: International Journal of Molecular Sciences

    Article Title: The Potential of Single-Transcription Factor Gene Expression by RT-qPCR for Subtyping Small Cell Lung Cancer

    doi: 10.3390/ijms26031293

    Figure Lengend Snippet: Cell morphology of mouse SCLC cell lines. Representative light microscopy images showing the growth patterns and cell morphology of mouse SCLC cells. Scale bars: 20 μm.

    Article Snippet: Human SCLC cell lines, including H69 (ATCC number: HTB-119, RRID: CVCL_1579), Shp77 (ATCC number: CRL-2195, RRID: CVCL_1693), H748 (ATCC number: CRL-5841, RRID: CVCL_1588), H345 (ATCC number: HTB-180, RRID: CVCL_1558), H82 (ATCC number: HTB-175, RRID: CVCL_1591), H1048 (ATCC number: CRL-5853, RRID: CVCL_1453), H526 (ATCC number: HTB-119, RRID: CVCL_1569), and H196 (ATCC number: HTB-119, RRID: CVCL_1509), were obtained from the American Type Culture Collection (ATCC), while the DMS273 (ECACC number: 95,062,830, RRID: CVCL_1176), cell line was obtained from the European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Light Microscopy

    Subtype classification of mouse SCLC cell lines by RT-qPCR. Basal mRNA expression levels of Ascl1 , Neurod1 , and Pou2f3 in mouse SCLC cell lines were measured as 1/ΔCt (Ct gene−Ct Gapdh ), with Gapdh as the housekeeping gene. Cells were plated and cultured for 48 h prior to RNA extraction. The plots represent the mean ± SD of three biological replicates for each cell line.

    Journal: International Journal of Molecular Sciences

    Article Title: The Potential of Single-Transcription Factor Gene Expression by RT-qPCR for Subtyping Small Cell Lung Cancer

    doi: 10.3390/ijms26031293

    Figure Lengend Snippet: Subtype classification of mouse SCLC cell lines by RT-qPCR. Basal mRNA expression levels of Ascl1 , Neurod1 , and Pou2f3 in mouse SCLC cell lines were measured as 1/ΔCt (Ct gene−Ct Gapdh ), with Gapdh as the housekeeping gene. Cells were plated and cultured for 48 h prior to RNA extraction. The plots represent the mean ± SD of three biological replicates for each cell line.

    Article Snippet: Human SCLC cell lines, including H69 (ATCC number: HTB-119, RRID: CVCL_1579), Shp77 (ATCC number: CRL-2195, RRID: CVCL_1693), H748 (ATCC number: CRL-5841, RRID: CVCL_1588), H345 (ATCC number: HTB-180, RRID: CVCL_1558), H82 (ATCC number: HTB-175, RRID: CVCL_1591), H1048 (ATCC number: CRL-5853, RRID: CVCL_1453), H526 (ATCC number: HTB-119, RRID: CVCL_1569), and H196 (ATCC number: HTB-119, RRID: CVCL_1509), were obtained from the American Type Culture Collection (ATCC), while the DMS273 (ECACC number: 95,062,830, RRID: CVCL_1176), cell line was obtained from the European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Quantitative RT-PCR, Expressing, Cell Culture, RNA Extraction

    Subtype classification of PDX and CDX SCLC models by RT-qPCR and IHC. ( A ) Basal relative mRNA expression levels of ASCL1 , NEUROD1, and POU2F3 in PDX and CDX models were assessed using RT-qPCR. Gene expression is shown as 1/ΔCt (Ct gene−Ct Housekeeping), with TOP1 used as the housekeeping gene for PDX1 and CDX13, and TUBB for the remaining samples. Cell lines Shp77, H82, and H1048 served as positive controls for ASCL1 , NEUROD1, and POU2F3 , respectively, while H841 was used as a control for triple-negative samples. Data are shown as the mean ± SD of three technical replicates for each sample. ( B ) Representative IHC images show staining for ASCL1 , NEUROD1 , and POU2F3 in SCLC PDX and CDX models. The most prevalent marker was used to define the subtype. PDX-1, CDX-13, and PDX-3 were negative for all three markers. Staining was visualized using 3,3′-Diaminobenzidine (DAB) as the chromogen. Scale bar = 50 µm.

    Journal: International Journal of Molecular Sciences

    Article Title: The Potential of Single-Transcription Factor Gene Expression by RT-qPCR for Subtyping Small Cell Lung Cancer

    doi: 10.3390/ijms26031293

    Figure Lengend Snippet: Subtype classification of PDX and CDX SCLC models by RT-qPCR and IHC. ( A ) Basal relative mRNA expression levels of ASCL1 , NEUROD1, and POU2F3 in PDX and CDX models were assessed using RT-qPCR. Gene expression is shown as 1/ΔCt (Ct gene−Ct Housekeeping), with TOP1 used as the housekeeping gene for PDX1 and CDX13, and TUBB for the remaining samples. Cell lines Shp77, H82, and H1048 served as positive controls for ASCL1 , NEUROD1, and POU2F3 , respectively, while H841 was used as a control for triple-negative samples. Data are shown as the mean ± SD of three technical replicates for each sample. ( B ) Representative IHC images show staining for ASCL1 , NEUROD1 , and POU2F3 in SCLC PDX and CDX models. The most prevalent marker was used to define the subtype. PDX-1, CDX-13, and PDX-3 were negative for all three markers. Staining was visualized using 3,3′-Diaminobenzidine (DAB) as the chromogen. Scale bar = 50 µm.

    Article Snippet: Human SCLC cell lines, including H69 (ATCC number: HTB-119, RRID: CVCL_1579), Shp77 (ATCC number: CRL-2195, RRID: CVCL_1693), H748 (ATCC number: CRL-5841, RRID: CVCL_1588), H345 (ATCC number: HTB-180, RRID: CVCL_1558), H82 (ATCC number: HTB-175, RRID: CVCL_1591), H1048 (ATCC number: CRL-5853, RRID: CVCL_1453), H526 (ATCC number: HTB-119, RRID: CVCL_1569), and H196 (ATCC number: HTB-119, RRID: CVCL_1509), were obtained from the American Type Culture Collection (ATCC), while the DMS273 (ECACC number: 95,062,830, RRID: CVCL_1176), cell line was obtained from the European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Quantitative RT-PCR, Expressing, Gene Expression, Control, Staining, Marker

    PTPMT1 knockdown reduces cell growth in A549 cells. PTPMT1 mRNA expression (A) and protein level (B) were significantly decreased in PTPMT1-shRNA-transfected cells. (C) CCK-8 assay for cell proliferation of PTPMT1-shRNA-transduced A549. (D) CCK-8 assay for cell proliferation of PTPMT1-shRNA-transduced H69 cells. ***, P<0.001, vs . scramble (control). PTPMT1, protein tyrosine phosphatase mitochondrial 1; mRNA, messenger RNA; CCK-8, cell counting kit 8; shRNA, short-hairpin RNA.

    Journal: Translational Cancer Research

    Article Title: PTPMT1 inhibition induces apoptosis and growth arrest of human SCLC cells by disrupting mitochondrial metabolism

    doi: 10.21037/tcr-2024-2379

    Figure Lengend Snippet: PTPMT1 knockdown reduces cell growth in A549 cells. PTPMT1 mRNA expression (A) and protein level (B) were significantly decreased in PTPMT1-shRNA-transfected cells. (C) CCK-8 assay for cell proliferation of PTPMT1-shRNA-transduced A549. (D) CCK-8 assay for cell proliferation of PTPMT1-shRNA-transduced H69 cells. ***, P<0.001, vs . scramble (control). PTPMT1, protein tyrosine phosphatase mitochondrial 1; mRNA, messenger RNA; CCK-8, cell counting kit 8; shRNA, short-hairpin RNA.

    Article Snippet: NCI-H69 (a human SCLC cell line) was purchased from Procell (Wuhan, China) and cultured in 1640 medium (Gibco, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS) (Gibco).

    Techniques: Knockdown, Expressing, shRNA, Transfection, CCK-8 Assay, Control, Cell Counting

    PTPMT1 inhibition induces cell death in A549 cells. (A,B) The percentage of apoptosis in the A549 and H69 cells transduced with PTPMT1-shRNA or control shRNA assessed by annexin-V assay and flow cytometry. ***, P<0.0001, sh-PTPMT1 vs . scramble (control). (C) The cell viability of A549 cells treated with alexidine dihydrochloride in the presence of Fer-1. (D) The cell viability of H69 cells treated with alexidine dihydrochloride in the presence of Fer-1. ns, no significance; **, P<0.01, alexidine dihydrochloride 2.5 µM vs . control (DMSO); ***, P<0.001, alexidine dihydrochloride 5 µM/10 µM vs . control (DMSO). PTPMT1, protein tyrosine phosphatase mitochondrial 1; shRNA, short-hairpin RNA; DMSO, dimethylsulfoxide.

    Journal: Translational Cancer Research

    Article Title: PTPMT1 inhibition induces apoptosis and growth arrest of human SCLC cells by disrupting mitochondrial metabolism

    doi: 10.21037/tcr-2024-2379

    Figure Lengend Snippet: PTPMT1 inhibition induces cell death in A549 cells. (A,B) The percentage of apoptosis in the A549 and H69 cells transduced with PTPMT1-shRNA or control shRNA assessed by annexin-V assay and flow cytometry. ***, P<0.0001, sh-PTPMT1 vs . scramble (control). (C) The cell viability of A549 cells treated with alexidine dihydrochloride in the presence of Fer-1. (D) The cell viability of H69 cells treated with alexidine dihydrochloride in the presence of Fer-1. ns, no significance; **, P<0.01, alexidine dihydrochloride 2.5 µM vs . control (DMSO); ***, P<0.001, alexidine dihydrochloride 5 µM/10 µM vs . control (DMSO). PTPMT1, protein tyrosine phosphatase mitochondrial 1; shRNA, short-hairpin RNA; DMSO, dimethylsulfoxide.

    Article Snippet: NCI-H69 (a human SCLC cell line) was purchased from Procell (Wuhan, China) and cultured in 1640 medium (Gibco, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS) (Gibco).

    Techniques: Inhibition, Transduction, shRNA, Control, Annexin V Assay, Flow Cytometry

    PTPMT1 inhibition reduces Glut expression. (A-E) The qRT-PCR analysis of the transcriptome differentially sequenced genes in H69 cells. *, P<0.05; **, P<0.01; ***, P<0.001, AD 5 µM vs . control (DMSO). (F,G) The H69 cells were transduced with PTPMT1 shRNA. The expression of Glut1 and Glut3 was determined by qRT-PCR. ***, P<0.001, sh-PTPMT1 vs . scramble (control). (H) The H69 cells were transduced with PTPMT1-shRNA or control vectors, and stained with JC-1 dye, and the ratio of the average fluorescence intensity of red/green was determined by flow cytometry. ***, P<0.001, sh-PTPMT1 vs . scramble (control). PTPMT1, protein tyrosine phosphatase mitochondrial 1; qRT-PCR, quantitative real-time polymerase chain reaction; shRNA, short-hairpin RNA; DMSO, dimethylsulfoxide; AD, alexidine dihydrochloride; mRNA, messenger RNA.

    Journal: Translational Cancer Research

    Article Title: PTPMT1 inhibition induces apoptosis and growth arrest of human SCLC cells by disrupting mitochondrial metabolism

    doi: 10.21037/tcr-2024-2379

    Figure Lengend Snippet: PTPMT1 inhibition reduces Glut expression. (A-E) The qRT-PCR analysis of the transcriptome differentially sequenced genes in H69 cells. *, P<0.05; **, P<0.01; ***, P<0.001, AD 5 µM vs . control (DMSO). (F,G) The H69 cells were transduced with PTPMT1 shRNA. The expression of Glut1 and Glut3 was determined by qRT-PCR. ***, P<0.001, sh-PTPMT1 vs . scramble (control). (H) The H69 cells were transduced with PTPMT1-shRNA or control vectors, and stained with JC-1 dye, and the ratio of the average fluorescence intensity of red/green was determined by flow cytometry. ***, P<0.001, sh-PTPMT1 vs . scramble (control). PTPMT1, protein tyrosine phosphatase mitochondrial 1; qRT-PCR, quantitative real-time polymerase chain reaction; shRNA, short-hairpin RNA; DMSO, dimethylsulfoxide; AD, alexidine dihydrochloride; mRNA, messenger RNA.

    Article Snippet: NCI-H69 (a human SCLC cell line) was purchased from Procell (Wuhan, China) and cultured in 1640 medium (Gibco, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS) (Gibco).

    Techniques: Inhibition, Expressing, Quantitative RT-PCR, Control, Transduction, shRNA, Staining, Fluorescence, Flow Cytometry, Real-time Polymerase Chain Reaction

    - Differential transcripts between small cell lung cancer (SCLC) and lung squamous cell carcinoma (LUSC), and between SCLC and lung adenocarcinoma (LUAD), and the overlapping targets based on the GSE40275 dataset. The volcano maps showing the differential transcripts between A ) SCLC and LUSC; and B ) between SCLC and LUSC, based on the GSE40275 dataset. The GEO2R tool was used to identify differentially expressed genes. The Venn diagram showing the overlapped C ) up-regulated transcripts; and D ) down-regulated transcripts among the differential transcripts described in A & B . E ) GO enrichment of the overlapped differentially expressed transcripts described in C & D . The plot was calculated and drawn by Metascape Gene List Analysis. LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - Differential transcripts between small cell lung cancer (SCLC) and lung squamous cell carcinoma (LUSC), and between SCLC and lung adenocarcinoma (LUAD), and the overlapping targets based on the GSE40275 dataset. The volcano maps showing the differential transcripts between A ) SCLC and LUSC; and B ) between SCLC and LUSC, based on the GSE40275 dataset. The GEO2R tool was used to identify differentially expressed genes. The Venn diagram showing the overlapped C ) up-regulated transcripts; and D ) down-regulated transcripts among the differential transcripts described in A & B . E ) GO enrichment of the overlapped differentially expressed transcripts described in C & D . The plot was calculated and drawn by Metascape Gene List Analysis. LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques:

    - MTHFD1 was higher expressed in small cell lung cancer (SCLC) tissues than lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) tissues. Comparing the mRNA levels of DNMT1 , MAT2A , HDAC5 , METTL3 , MECP2 , and MTHFD1 between: A ) SCLC tissues (n=6) and LUSC tissues (n=6); and B ) between SCLC tissues (n=6) and LUAD tissues (n=6) in a small-scale samples. C ) Comparing the MTHFD1 levels between tumor tissues and matched adjacent tissues in LUSC (left, n=56), LUAD (middle, n=70), and SCLC (right, n=70) cases in a large-scale samples. D ) Comparing the MTHFD1 levels in tissues from healthy controls (HCs, n=33), LUSC (n=56), LUAD (n=70), and SCLC (n=70) cases in a large-scale samples. E-I ) The receiver operating characteristic curve for the MTHFD1 levels in distinguishing: E ) LUSCs and HCs; F ) LUADs and HCs; G ) SCLCs and HCs; H ) SCLC and LUSCs; and I ) SCLC and LUADs. Left: representative stained images among these 4 groups, right: bar chart comparison of differences among these 4 groups, HCs: healthy controls, LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - MTHFD1 was higher expressed in small cell lung cancer (SCLC) tissues than lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) tissues. Comparing the mRNA levels of DNMT1 , MAT2A , HDAC5 , METTL3 , MECP2 , and MTHFD1 between: A ) SCLC tissues (n=6) and LUSC tissues (n=6); and B ) between SCLC tissues (n=6) and LUAD tissues (n=6) in a small-scale samples. C ) Comparing the MTHFD1 levels between tumor tissues and matched adjacent tissues in LUSC (left, n=56), LUAD (middle, n=70), and SCLC (right, n=70) cases in a large-scale samples. D ) Comparing the MTHFD1 levels in tissues from healthy controls (HCs, n=33), LUSC (n=56), LUAD (n=70), and SCLC (n=70) cases in a large-scale samples. E-I ) The receiver operating characteristic curve for the MTHFD1 levels in distinguishing: E ) LUSCs and HCs; F ) LUADs and HCs; G ) SCLCs and HCs; H ) SCLC and LUSCs; and I ) SCLC and LUADs. Left: representative stained images among these 4 groups, right: bar chart comparison of differences among these 4 groups, HCs: healthy controls, LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques: Staining, Comparison

    - Clinical indications for included lung cancer patients.

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - Clinical indications for included lung cancer patients.

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques:

    - Association of MTHFD1 levels with clinical indications for small cell lung cancer, lung squamous cell carcinoma and lung adenocarcinoma patients.

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - Association of MTHFD1 levels with clinical indications for small cell lung cancer, lung squamous cell carcinoma and lung adenocarcinoma patients.

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques:

    - MTHFD1 levels were specifically associated with prognosis of small cell lung cancer (SCLC) patients after chemoradiotherapy treatment. Kaplan-Meier curves for time to 2-year overall survival of patients with: A ) SCLC; B ) lung squamous cell carcinoma; and C ) lung adenocarcinoma according to MTHFD1 levels. LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer, OS: overall survival

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - MTHFD1 levels were specifically associated with prognosis of small cell lung cancer (SCLC) patients after chemoradiotherapy treatment. Kaplan-Meier curves for time to 2-year overall survival of patients with: A ) SCLC; B ) lung squamous cell carcinoma; and C ) lung adenocarcinoma according to MTHFD1 levels. LUSC: lung squamous cell carcinoma, LUAD: lung adenocarcinoma, SCLC: small cell lung cancer, OS: overall survival

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques:

    - Overexpression of MTHFD1 increases radio-resistance in both small cell lung cancer and non-small cell lung cancer in vitro. A ) MTHFD1 levels were determined in H69, A549, and BEAS-2B cells. B-C ) The H69 and A549 cells were instantly transfected with MTHFD1 over-expressed plasmid for 24 hours, and then the viable cells of B ) H69; and C ) A549 were detected after treated by different dose irradiation. D-E ) The H69 and A549 cells were instantly transfected with MTHFD1 over-expressed plasmid and control plasmid for 24 hours, and then the apoptosis rate of B ) H69; and C ) A549 were detected after treated by different dose irradiation.

    Journal: Saudi Medical Journal

    Article Title: Specific association of MTHFD1 expressions with small cell lung cancer development and chemoradiotherapy outcome

    doi: 10.15537/smj.2024.45.8.20230990

    Figure Lengend Snippet: - Overexpression of MTHFD1 increases radio-resistance in both small cell lung cancer and non-small cell lung cancer in vitro. A ) MTHFD1 levels were determined in H69, A549, and BEAS-2B cells. B-C ) The H69 and A549 cells were instantly transfected with MTHFD1 over-expressed plasmid for 24 hours, and then the viable cells of B ) H69; and C ) A549 were detected after treated by different dose irradiation. D-E ) The H69 and A549 cells were instantly transfected with MTHFD1 over-expressed plasmid and control plasmid for 24 hours, and then the apoptosis rate of B ) H69; and C ) A549 were detected after treated by different dose irradiation.

    Article Snippet: The human SCLC cell line H69, NSCLC cell line A549, and normal lung epithelial cell line BEAS-2B were purchased from the American Type Culture Collection (ATCC, USA).

    Techniques: Over Expression, In Vitro, Transfection, Plasmid Preparation, Irradiation, Control