Loss of SETD2 aggravates colorectal cancer progression caused by SMAD4 deletion through the RAS/MAPK pathway [ChIP-seq]
To investigate the function of SETD2 in SMAD4-mutant colorectal cancer, we induced colorectal cancer in mice with intestinal epithelium-specific knockout of SMAD4 and SETD2 using AOM/DSS treatment. Overall design: Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) was used to detect H3K36me3 histone modification in the intestinal epithelial cells of SMAD4 knockout mice after AOM/DSS treatment.