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

