Integrated Analysis of Genes Encoding ATP-Dependent Chromatin Remodelers Identifies CHD7 as a Potential Target for Colorectal Cancer Therapy

We experimentally demonstrated that CHD7 promotes the growth of colorectal cancer cells in vitro and in vivo. Mechanistically, RNA-seq and ATAC-seq approaches together with ChIP assays indicated that CHD7 can bind to the promoters of target genes to maintain chromatin accessibility and facilitate transcription. We found that CHD7 knockdown downregulates AK4 expression and activates AMPK phosphorylation, thereby promoting the phosphorylation and stability of p53 and leading to the inhibition of the colorectal cancer growth. Our genomic analyses of ATPCRs across large-scale cancer specimens identified potential therapeutic targets and our experimental studies revealed a novel CHD7-AK4-AMPK-p53 axis that plays an oncogenic role in colorectal cancer. Examination of chromatin accessibility changes in CHD7 knockdown and control RKO cells.