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野生型p53诱导的磷酸酶1在癌症中的作用。

Role of wild-type p53-induced phosphatase 1 in cancer.

作者信息

Wang Zhi-Peng, Tian Ye, Lin Jun

机构信息

Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.

出版信息

Oncol Lett. 2017 Oct;14(4):3893-3898. doi: 10.3892/ol.2017.6685. Epub 2017 Jul 27.

Abstract

Wild-type p53-induced phosphatase (Wip1) is a member of the protein phosphatase type 2C family and is an established oncogene due to its dephosphorylation of several tumor suppressors and negative control of the DNA damage response system. It has been reported to dephosphorylate p53, ataxia telangiectasia mutated, checkpoint kinase 1 and p38 mitogen activated protein kinases, forming negative feedback loops to inhibit apoptosis and cell cycle arrest. Wip1 serves a major role in tumorigenesis, progression, invasion, distant metastasis and apoptosis in various types of human cancer. Therefore, it may be a potential biomarker and therapeutic target in the diagnosis and treatment of cancer. Furthermore, previous evidence has revealed a new role for Wip1 in the regulation of chemotherapy resistance. In the present review, the current knowledge on the role of Wip1 in cancer is discussed, as well as its potential as a novel target for cancer treatment and its function in chemotherapy resistance.

摘要

野生型p53诱导磷酸酶(Wip1)是2C型蛋白磷酸酶家族的成员,由于它能使多种肿瘤抑制因子去磷酸化并对DNA损伤反应系统进行负调控,因此是一种公认的癌基因。据报道,它能使p53、共济失调毛细血管扩张症突变基因、关卡激酶1和p38丝裂原活化蛋白激酶去磷酸化,形成负反馈环以抑制细胞凋亡和细胞周期停滞。Wip1在各类人类癌症的肿瘤发生、进展、侵袭、远处转移和细胞凋亡中起主要作用。因此,它可能是癌症诊断和治疗中的一个潜在生物标志物和治疗靶点。此外,先前的证据揭示了Wip1在化疗耐药性调控中的新作用。在本综述中,我们讨论了目前关于Wip1在癌症中的作用的知识,以及它作为癌症治疗新靶点的潜力及其在化疗耐药性中的功能。

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