A broad role of KMT2C/MLL3 in the transcriptional regulation of DNA repair components in cancer ChIPseq

Genome-wide studies in tumor cells have indicated that chromatin-modifying proteins are commonly mutated in human cancers. The lysine-specific methyltransferase 2C (KMT2C/MLL3) is a putative tumor suppressor in several epithelia and in myeloid cells. Downregulation of KMT2C in bladder cancer cells leads to extensive changes in the epigenetic and expression status of DNA damage response and DNA repair genes. More specifically, cells with low KMT2C activity are deficient in homologous recombination-mediated double strand break DNA repair. Consequently, these cells suffer from substantially higher endogenous DNA damage and genomic instability.