PTEN: Its deregulation and tumorigenesis
PTEN: Its deregulation and tumorigenesis
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DOI：
10.1248/bpb.30.1624
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发表时间：
2007-09-01
影响因子：
2
通讯作者：
Maehama, Tomohiko
中科院分区：
文献类型：
--
作者：
Maehama, Tomohiko
肿瘤抑制性磷酸酶和张力蛋白同源物（PTEN）作为磷酸肌醇3-磷酸酶起作用，其拮抗磷脂酰肌醇3-激酶作用，并负调节细胞增殖和存活信号。失活的PTEN功能突变引起细胞的过度增殖失调，导致致癌转化。最近的研究已经确定了一些上游调控因子的PTEN和揭示，在PTEN调控系统的损伤可能成为致癌转化的细胞的一个致病因素。本文就与人类肿瘤发生相关的PTEN失活机制进行综述，重点介绍近年来PTEN调控因子的研究进展。
The tumor suppressor phosphatase and tensin homolog (PTEN) functions as a phosphoinositide 3-phosphatase, that antagonizes phosphatidylinositol 3-kinase action, and negatively regulates cell proliferation and survival signals. Inactivation of PTEN by loss-of-function mutations gives rise to deregulated hyperproliferation of cells, leading to oncogenic transformation. Recent studies have identified a number of upstream regulatory factors for PTEN and unveiled that the impairment in the PTEN regulatory system potentially becomes a causal factor for oncogenic transformation of cells. This article will review the PTEN inactivation mechanism which is linked to human tumorigenesis, particularly focusing on recent research progress in PTEN regulators.