[Research progress on the expression and carcinogenic mechanisms of SETD2 in malignant tumors].

表观遗传学 生物 组蛋白 癌症研究 癌症表观遗传学 表观遗传学 染色质 组蛋白甲基转移酶 遗传学 DNA甲基化 基因 基因表达
作者
Ming Yu,X Zhang
出处
期刊:PubMed [National Institutes of Health]
卷期号:39 (1): 73-77 被引量:1
标识
DOI:10.3760/cma.j.cn121094-20191129-00550
摘要

The human epigenetic gene of SET domain containing 2 (SETD2) is located at the cytogenetic band p21.31 of chromosome 3, which encodes the histone3 lysine36 trimethyltransferase SETD2, the major enzyme that catalyzes the trimethylation of lysine 36 on histone 3 (H3K36me3) of human. SETD2 involves in many pathologic and physiological processes such as transcriptional elongation, DNA damage repair, alternative splicing, epigenetic modifications of gene expression, viral immunology, embryonic development, and angiogenesis. A growing list of tumor types including renal cell carcinoma and mesothelioma develops with mutation or inactivation of SETD2. SETD2 loss-of-function promotes the occurrences and development of cancers by inhibiting process of transcription extension, damage repair, cell cycles, apoptosis and cell metabolism. The under expression and mutation of SETD2 is synthetically lethal with the inhibition of G2M checkpoint and PI3K-AKT pathway and SETD2 is considered as a potential epigenetic therapy targets. Furthermore, a loss of SETD2 indicates worse pathological features. There are huge prospects in the diagnosis and treatment of related cancers.
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