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ZNF296 drives immune evasion in epithelial cancer cells [ChIP-seq]

GSE283059 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2025/09/06 Platform GPL24676
Summary
Using a genome-wide CRISPR activation screen, we identified ZNF296, a transcription factor highly expressed in epithelial cancers, as a key regulator of tumor resistance to NK cell-mediated cytotoxicity. To uncover its direct targets, we performed ChIP-seq in A549 cells overexpressing ZNF296-Flag, revealing its preferential binding to specific genomic regions. IP-MS further demonstrated that ZNF296 interacts with the NuRD complex, which suppresses gene expression via histone deacetylase activity.To test whether ZNF296 mediates transcriptional repression through the NuRD complex, we conducted ChIP-seq for HDAC1, a core component of the complex, in ZNF296-overexpressing (ZNF296-OE) and control A549 cells. These analyses revealed genomic targets co-regulated by ZNF296 and the NuRD complex, providing insights into its mechanism of transcriptional regulation.
Published in
ZNF296 Drives Immune Evasion in Epithelial Cancers by Repressing Immune Stimulatory Genes
Wang H, Zhao F, Li Y et al. · Cancer research 2026 · PMID 40991281 · doi:10.1158/0008-5472.CAN-25-0153
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Also filed as BioProject PRJNA1191519 and SRA study SRP548097. Searching any of these in the dataset finder brings you back here.

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