ZNF296 drives immune evasion in epithelial cancer cells [ATAC-seq]
Using a genome-wide CRISPR activation screen, we identified ZNF296, a transcription factor prominently expressed in epithelial cancers, as a key regulator of tumor resistance to NK cell-mediated cytotoxicity. To investigate the role of ZNF296 in regulating chromatin accessibility and its effects on gene transcription, we performed ATAC-seq on ZNF296-overexpressing (ZNF296-OE) and control A549 cells. These data provide insights into the epigenetic mechanisms underlying ZNF296-mediated tumor immune evasion. Overall design: To identify ZNF296-dependent chromatin accessibility, ATAC-seq was performed on A549 cells with control and ZNF296 overexpression. ZNF296-overexpressing A549 cells were generated by introducing ZNF296 ORF.