High-throughput sequencing in ARID1A knockout MDA-MB-231 cells [H3K4me3 histone modification ChIP-seq]

ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high-throughput sequencing (ChIP–seq) to investigate H3K4me3 histone modification of ARID1A knockout and control MDA-MB-231 cells. Overall design: We performed H3K4me3 ChIP-seq in ARID1A knockout and control MDA-MB-231 cells.