Loss of Ezh2 function reshapes DNA replication initiation landscape
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA847445 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19594474.fastq.gz | Fastqsanger.gz | |||
| SRR19594475.fastq.gz | Fastqsanger.gz | |||
| SRR19594476.fastq.gz | Fastqsanger.gz | |||
| SRR19594477.fastq.gz | Fastqsanger.gz | |||
| SRR19594478.fastq.gz | Fastqsanger.gz |
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Project 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.
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