USP7在前列腺癌发病机制中的研究  

The mechanism of USP7 in prostate cancer

作　　者：尹汝莎 傅强[1] 张克勤[1] 张辉[1] 孙鼎琪[1] 朱爱云[1] 刘帅[1] Yin Rusha;Fu Qiang;Zhang Keqin;Zhang Hui;Sun Dingqi;Zhu Aiyun;Liu Shuai(Department of Urology,Shandong Provincial Hospital Affiliated to Shandong University,Jinan 250021,China)

机构地区：[1]山东大学附属省立医院泌尿外科,济南250021

出　　处：《中华泌尿外科杂志》2020年第7期555-558,共4页Chinese Journal of Urology

基　　金：济南市科技计划(201907062)。

摘　　要：去势抵抗性前列腺癌(CRPC)的产生使前列腺癌传统的内分泌疗法受到挑战,越来越多的研究转向从分子水平寻找合适的靶点来抑制癌症的进展。泛素特异性蛋白酶7(USP7)是一种重要的去泛素化酶,以翻译后修饰的方式调控关键蛋白的半衰期或亚细胞定位。近期的研究结果表明,USP7在前列腺癌细胞中显示出明显的促癌效应,但机制复杂,本文对USP7在前列腺癌中的作用机制进行综述。The traditional androgen deprivation therapy has been challenged since the appearance of castration resistant prostate cancer(CRPC).More and more researches are focusing on searching the proper molecular target to inhibit the progression of tumors.Ubiquitin specific protease 7(USP7),as an important deubiquitinating enzyme,regulates the half-life or subcellular localization of key proteins via posttranslational modification.It has been reported recently that prostate cancer cells are suppressed by USP7 inhibitors,but the complicated mechanisms remain to clarify.In this paper,we review the mechanism of USP7 in prostate cancer,suggesting the potential value of USP7 inhibitors in the treatment of CRPC.

关 键 词：前列腺肿瘤 去势抵抗 泛素特异性蛋白酶7 雄激素受体 

分 类 号：R737.25[医药卫生—肿瘤]