Home > Browse Issues > Vol.37 No.4
Research Progress of Histone Methyl-transferase SETD2
Wang Xiaofang, Dong Fang, Wang Yajie, Cheng Tao*
State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China
Abstract: SETD2 is an epigenetic gene encoding the H3K36-specific histone methyl-transferase. It plays important roles in gene transcription enlongation and mismatch repair through interacting with RNA polymerase II in cells. Disruption of SETD2 in mice results in defects in vascular remodeling via H3K36me3 down-regulation. It has been shown that many human tumors (e.g. breast cancer， renal carcinoma and bladder carcinoma) have SETD2 alternations. Recent studies showed that down-regulation of SETD2 contributed to both initiation and progression during leukemia development by enhancing self-renewal potential of leukemia stem cells. The existence of SETD2 mutations in a range of human tumors suggests that disruption of the SETD2-H3K36me3 pathway is a distinct epigenetic mechanism for cancer development， thereby offering a new opportunity for the development of cancer diagnostics and therapeutics. However， how disruption of SETD2 cooperates with other pathogenic mechanisms， will certainly need further investigation. In this review， we first introduce the structure and function of SETD2 molecule， and then focus on its roles in embryonic development and human cancers， especially leukemia.
CN
EN