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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

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    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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    A, YAP1 protein levels in H69 and H69/CPR cells and tumors following cisplatin treatment by RPPA. B, Extended treatment of <t>SCLC</t> <t>cell</t> lines with cisplatin decreases ASCL1 and increases YAP1 and NOTCH2 levels. C, Bulk RNAseq analysis of YAP1 (left) and YAP/TAZ target score in SCLC patient tumors at treatment naïve and relapsed timepoints. D, Representative IHC demonstrating nuclear YAP1 in SCLC cells from a relapsed pure SCLC tumor (left) and in a mixed histology tumor (right). Scale bar = 100 or 500 μm. G, YAP1 promoter methylation correlates with YAP1 expression in SCLC patient biopsies. H, ctDNA levels are unchanged between baseline and relapsed samples (left), but YAP1 promoter methylation is detectable only in baseline samples (right).
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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

    A, YAP1 protein levels in H69 and H69/CPR cells and tumors following cisplatin treatment by RPPA. B, Extended treatment of SCLC cell lines with cisplatin decreases ASCL1 and increases YAP1 and NOTCH2 levels. C, Bulk RNAseq analysis of YAP1 (left) and YAP/TAZ target score in SCLC patient tumors at treatment naïve and relapsed timepoints. D, Representative IHC demonstrating nuclear YAP1 in SCLC cells from a relapsed pure SCLC tumor (left) and in a mixed histology tumor (right). Scale bar = 100 or 500 μm. G, YAP1 promoter methylation correlates with YAP1 expression in SCLC patient biopsies. H, ctDNA levels are unchanged between baseline and relapsed samples (left), but YAP1 promoter methylation is detectable only in baseline samples (right).

    Journal: bioRxiv

    Article Title: YAP1 defines an emergent, plastic population of relapsed small cell lung cancer

    doi: 10.1101/2025.10.21.683746

    Figure Lengend Snippet: A, YAP1 protein levels in H69 and H69/CPR cells and tumors following cisplatin treatment by RPPA. B, Extended treatment of SCLC cell lines with cisplatin decreases ASCL1 and increases YAP1 and NOTCH2 levels. C, Bulk RNAseq analysis of YAP1 (left) and YAP/TAZ target score in SCLC patient tumors at treatment naïve and relapsed timepoints. D, Representative IHC demonstrating nuclear YAP1 in SCLC cells from a relapsed pure SCLC tumor (left) and in a mixed histology tumor (right). Scale bar = 100 or 500 μm. G, YAP1 promoter methylation correlates with YAP1 expression in SCLC patient biopsies. H, ctDNA levels are unchanged between baseline and relapsed samples (left), but YAP1 promoter methylation is detectable only in baseline samples (right).

    Article Snippet: Human SCLC cell lines were purchased from ATCC.

    Techniques: Methylation, Expressing

    - 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