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EZH2 inhibition reshapes 3D chromatin architecture to induce immunogenic phenotype in small cell lung cancer [ATAC-Seq]

GSE329204 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2026/04/27 Platform GPL24676
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE329204_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1458137 and SRA study SRP695248. Searching any of these in the dataset finder brings you back here.

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