ZNF296 drives immune evasion in epithelial cancer cells [ChIP-seq]
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. Overall design: ChIP-seq was performed in A549 cells overexpressing ZNF296-Flag using anti-Flag antibodies to identify direct genomic targets of ZNF296. ChIP-seq for HDAC1 was also conducted in ZNF296-OE and control A549 cells to determine co-regulation by ZNF296 and the NuRD complex.