<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329205/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329205</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>EZH2 inhibition reshapes 3D chromatin architecture to induce immunogenic phenotype in small cell lung cancer [RNA-Seq]</name><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 RNA‑sequencing dataset.</description><dates><publication>2026/04/27</publication></dates><accession>GSE329205</accession><cross_references><GSM>GSM9699250</GSM><GSM>GSM9699249</GSM><GSM>GSM9699254</GSM><GSM>GSM9699253</GSM><GSM>GSM9699252</GSM><GSM>GSM9699251</GSM><GPL>24676</GPL><GSE>329205</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>