small cell lung cancer sclc  (AMS Biotechnology)

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: Molecular Cancer Therapeutics

Article Title: OBI-992, a Novel TROP2-Targeted Antibody–Drug Conjugate, Demonstrates Antitumor Activity in Multiple Cancer Models

doi: 10.1158/1535-7163.MCT-24-0588

Figure Lengend Snippet: TROP2 expression in various cancer tissues. A, The expression levels of TROP2 in tissue samples from 19 cancer types were analyzed by IHC. Dots indicate TROP2 H -score for each sample, and solid bars indicate the median H -score of each cancer type. B, TROP2 prevalence rates ( x -axis) were calculated as the percentage of samples with TROP2 H -score ≥100. The ranking order of cancer types was based on the TROP2 prevalence rate. C, Plot of percentage of cells from tumor (blue) and corresponding normal tissues (gray) with TROP2 membrane expression determined by IHC. Each dot represents an individual sample. Solid bars indicate the median percent of TROP2-expressing cells for each tissue type. The numbers of specimens used for each cancer type are indicated in the plots. Representative IHC images of TROP2 high (3+), moderate (2+), and low (1+) expression are shown in Supplementary Fig. S3. Adeno, adenocarcinoma; BC, breast carcinoma; Ca., cancer/carcinoma; CRC, colorectal cancer; H&N, head and neck carcinoma; HER2, human epidermal growth factor receptor 2; HR, hormone receptor; HRPC, hormone-resistant prostate cancer; IHC, immunohistochemistry; NSCLC, non-small cell lung cancer; RCC, renal cell renal carcinoma; SCC, squamous carcinoma; SCLC, small cell lung carcinoma; TNBC, triple-negative breast carcinoma.

Article Snippet: Up to 448 formalin-fixed, paraffin-embedded human late-stage tumor tissue samples, representing 19 cancer types [bladder cancer, cervical adenocarcinoma, cervical squamous cell carcinoma (SCC), colorectal cancer, endometrial cancer, esophageal cancer, gallbladder cancer, gastric cancer, head and neck cancer, hormone receptor-positive (HR + ) breast cancer, human epidermal growth factor receptor 2-positive (HER2 + ) breast cancer, non-small cell lung cancer (NSCLC) adenocarcinoma, NSCLC SCC, ovarian adenocarcinoma, pancreatic cancer, prostate cancer, renal cell carcinoma (RCC), small cell lung cancer (SCLC), and triple-negative breast cancer (TNBC)], were purchased from AMS Biotechnology.

Techniques: Expressing, Membrane, Immunohistochemistry

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

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: O-GalNAc Glycosylation Activates MBL-Mediated Complement and Coagulation Cascades to Drive Organotropic Metastasis.

doi: 10.1002/advs.202504809

Figure Lengend Snippet: Figure 7. Blockade of O-GalNAc suppresses liver metastasis in a wide range of NE cancers. a–d) The O-GalNAc inhibitor benzyl-𝛼-GalNAc treatment leads to significantly reduced liver metastatic burdens in rb1Δ/Δp53Δ/Δ organoid-inoculated C57BL/6 mice (n = 7), as exemplified by representative H&E staining imagesscale bar = 5 mm) and quantification data. e-h) Benzyl-𝛼-GalNAc treatment results in significantly attenuated liver metastatic burdens in SCLC NCI-H82-inoculated nude mice (n = 6), as revealed by representative H&E staining images, scale bar = 5 mm) and quantification data. i–l) Benzyl-𝛼-GalNAc treatment leads to significantly repressed liver metastatic lesions in neuroendocrine colon cancer cell COLO-320DM inoculated nude mice (n = 4), as exemplified by representative H&E staining images, scale bar = 5 mm) and quantification results. For statistics in (d), (h), and (l) student’s t-test was applied and data were shown as mean ± SD. P value ≤0.01 was considered as statistically significant. For statistics in this figure, the two-tail unpaired Student’s-t test was applied for (d), (h) and (l). Data were shown as means ± SD.

Article Snippet: Human lung cancer cell lines included lung adenocarcinoma (LUAD) A549, small cell lung cancer (SCLC) NCI-H146, and NCI-H82, which were commercially available from ATCC.

Techniques: Staining