5-羟甲基胞嘧啶
癌变
DNA去甲基化
染色体易位
表观遗传学
去甲基化
癌症研究
DNA甲基化
基因
体细胞
致癌物
DNA
5-甲基胞嘧啶
机制(生物学)
细胞生物学
医学
生物
基因表达
遗传学
认识论
哲学
作者
Rui Wang,Jing Zhang,Jian Qi
标识
DOI:10.1016/j.cdtm.2019.12.001
摘要
Abstract Ten‐eleven translocation (TET) methylcytosine dioxygenases catalyze the oxidative reactions of 5‐methylcytosine (5‐mC) to 5‐hydroxymethylcytosine (5‐hmC), 5‐formylcytosine (5‐fC), and 5‐carboxylcytosine (5‐caC), which are intermediate steps during DNA demethylation. It is reported that somatic mutations of TET2 gene are identified in a variety of human tumors, especially in hematological malignancies. The tendency and mechanism of cellular differentiation in different systems are affected by TET2 via regulation of associated gene expression or maintenance of demethylated state. TET2 acts as a critical driver of tumorigenesis through the conversion of 5‐mC to 5‐hmC and successive oxidation products. Sometimes, it requires special interactions and cofactors. Here, we reviewed recent advances in understanding the function of TET2 proteins in regulating cell differentiation, and its role in various tumors focusing on several digestive cancers.
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