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

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

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

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

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

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

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

Journal: Cancer Biology & Medicine

Article Title: Chidamide suppresses macrophage-mediated immune evasion and tumor progression in small cell lung cancer by targeting the STAT4/CCL2 signaling pathway

doi: 10.20892/j.issn.2095-3941.2024.0241

Figure Lengend Snippet: Chidamide inhibits malignancy proliferation in SCLC. (A-F) Effects of chidamide on the viability of various neuroendocrine SCLC cells in vitro (A-C), subcutaneous tumor growth, and toxicity in vivo (D-F). (G, H) Expression of Ki-67 in the control and chidamide groups. (I) Gene set enrichment analysis (GSEA) of apoptosis pathway transcriptomic differences in SCLC cells in the chidamide and control groups. (J) Quantification of apoptosis-associated gene expression in the chidamide and control groups according to qPCR and WB. (K-M) Flow cytometry analyses of SCLC cell apoptosis after treatment with various chidamide concentrations. Bars represent the mean ± SD values. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Student’s t -test (E, H, J), one-way ANOVA (M). These experiments were performed three times.

Article Snippet: Human SCLC cell lines (SHP77, NCI-H889, NCI-H446, and DMS53), the human mononuclear cell line, THP1, and the murine macrophage cell line, RAW264.7, were obtained from the American Type Culture Collection (ATCC) (Manassas, VA, USA).

Techniques: In Vitro, In Vivo, Expressing, Control, Gene Expression, Flow Cytometry

Journal: Cancer Biology & Medicine

Article Title: Chidamide suppresses macrophage-mediated immune evasion and tumor progression in small cell lung cancer by targeting the STAT4/CCL2 signaling pathway

doi: 10.20892/j.issn.2095-3941.2024.0241

Figure Lengend Snippet: Chidamide promotes CCL2 expression in SCLC. (A) Differential gene expression changes in SHP77 and H889 cells before and after treatment with chidamide. KEGG signaling pathway enrichment in human (B) and murine SCLC cells (D) before and after chidamide treatment. Differential cytokine heatmap in cytokine-cytokine receptor interaction signaling pathways in human (C) and murine SCLC cells (E). (F) Venn diagram of the above-mentioned differentially expressed cytokines in the three SCLC cell lines. (G) Expression of three cytokines based on RNA sequencing. (H) Expression of three cytokines in SCLC cells verified by qPCR. (I) CCL2 expression between normal and SCLC tissues in the GSE43346 (43/25), GSE60052 (7/79), GSE15240 (3/38), and GSE149507 (18/18) datasets. (J) Survival curve of 81 SCLC patients with high or low CCL2 expression. (K-M) Changes in CCL2 expression in SCLC cells treated with chidamide for various times according to qPCR (K), ELISA (L), and WB (M). Bars represent the mean ± SD values. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Student’s t -test (G, H, I), one-way ANOVA (K, L). These experiments were performed three times (H, K, L, M).

Article Snippet: Human SCLC cell lines (SHP77, NCI-H889, NCI-H446, and DMS53), the human mononuclear cell line, THP1, and the murine macrophage cell line, RAW264.7, were obtained from the American Type Culture Collection (ATCC) (Manassas, VA, USA).

Techniques: Expressing, Gene Expression, Protein-Protein interactions, RNA Sequencing, Enzyme-linked Immunosorbent Assay

Journal: Oncogene

Article Title: Integrative epigenome and transcriptome analyses reveal transcriptional programs differentially regulated by ASCL1 and NEUROD1 in small cell lung cancer

doi: 10.1038/s41388-025-03481-2

Figure Lengend Snippet: A H3K4me3, H3K27ac, and H3K27me3 signals (expressed on the vertical axis) in the genomic regions around the ASCL1 and NEUROD1 gene loci of Lu134A, DMS53, DMS454, and WA-hT cells. The arrows indicate the transcripts of ASCL1 and NEUROD1 . Note that the starting point of each arrow corresponds to the transcription start site (TSS). B Distributions of H3K4me3 and H3K27ac signals within the intervals of 3.0 kb upstream of TSSs, gene bodies, and 3.0 kb downstream of transcription end sites (TESs) of the ASCL1 or NEUROD1 target genes in DMS53, DMS454, Lu134A, and WA-hT. The values on the Y -axis of the upper panels indicate normalised read counts. C Venn diagram showing overlap of known target genes of ASCL1 and NEUROD1 identified in SCLC-A and SCLC-N cell lines, respectively, and neighbouring genes of CUT&Tag peaks identified using CUT&Tag assay for ASCL1 and NEUROD1 in Lu134A cells. Numbers of genes are indicated.

Article Snippet: Human SCLC cell lines DMS53, DMS454, and H2066 were purchased from ATCC (Manassas, VA, USA).

Techniques: