作者: Yun Huang , Anjana Rao
DOI: 10.1016/J.TIG.2014.07.005
关键词:
摘要: DNA methylation has been linked to aberrant silencing of tumor suppressor genes in cancer, and an imbalance methylation–demethylation cycles is intimately implicated the onset progression tumors. Ten-eleven translocation (TET) proteins are Fe(II)- 2-oxoglutarate (2OG)-dependent dioxygenases that successively oxidize 5-methylcytosine (5mC) 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), 5-carboxylcytosine (5caC), thereby mediating active demethylation. In this review, we focus on pathophysiological role TET 5hmC cancer. We present overview loss-of-function mutations abnormal expression regulation hematological malignancies solid tumors, discuss potential prognostic value assessing levels cancer patients. also address crosstalk between two critical enzymes involved cell metabolism: O -linked β- N -acetylglucosamine transferase (OGT) isocitrate dehydrogenase (IDH). Lastly, therapeutic targeting