{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329204/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329204"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"EZH2 inhibition reshapes 3D chromatin architecture to induce immunogenic phenotype in small cell lung cancer [ATAC-Seq]","description":"EZH2, the enzymatic core of the Polycomb Repressive Complex 2 (PRC2), is overexpressed in small cell lung cancer (SCLC). Previous studies have shown that EZH2 enforces epigenetic silencing of immune and DNA repair genes, including Class I MHC molecules (HLA‑A/B/C) and SLFN11. To investigate how EZH1/2 inhibition reshapes the 3D chromatin landscape and its relationship to transcriptional regulation, we performed multi‑omic profiling of a neuroendocrine SCLC cell line (NCI‑H146) treated with the dual EZH1/2 inhibitor valemetostat for 9 days. We employed Micro‑C sequencing for high‑resolution 3D genome mapping, ATAC‑sequencing for chromatin accessibility profiling, and RNA‑sequencing for whole‑transcriptome analysis. This is the ATAC sequencing dataset.","dates":{"publication":"2026/04/27"},"accession":"GSE329204","cross_references":{"GSM":["GSM9699248","GSM9699247","GSM9699246","GSM9699245","GSM9699244","GSM9699243"],"GPL":["24676"],"GSE":["329204"],"taxon":["Homo sapiens"]}}