去泛素化酶OTUD3通过稳定PTEN抑制癌症发生发展  

Deubiquitylase OTUD3 Regulates PTEN Stability and Suppresses Tumorigenesis

作　　者：李洪昌[1] 张鹏飞[1] 袁林[1] 张令强[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所,北京蛋白质组研究中心,蛋白质组学国家重点实验室,肿瘤医学协同创新中心,北京100850

出　　处：《中国细胞生物学学报》2016年第6期657-661,共5页Chinese Journal of Cell Biology

基　　金：国家自然科学基金重点项目(批准号:31330021);北京市自然科学基金(批准号:5142020)资助的课题

摘　　要：PTEN(phosphatase and tension homology,deleted in chromosome 10)是重要的抑癌分子,其蛋白剂量水平的精细变化与肿瘤的发生发展密切相关。PTEN的蛋白水平调控研究一直是该领域的研究热点,虽然已经发现了数个PTEN的泛素连接酶,但能调控PTEN蛋白稳定性的去泛素化酶却一直不明确。该文介绍了PTEN泛素化修饰的最新进展,去泛素化酶OTUD3(OTU domaincontaining protein 3)通过去除PTEN的多聚泛素化维持其蛋白水平,并发挥抑癌功能。这一研究进展弥补了通过拮抗泛素化降解从而稳定PTEN这一长期未被阐释的调控机制。PTEN （phosphatase and tension homology, deleted in chromosome 10） is one of the most important tumor suppressors and a small quantity of reduction in PTEN protein level can lead to occurrence and development of tumors. The regulation of PTEN protein stability has been an attractive hotspot. Although several ubiquitin ligases for PTEN have been identified, the deubiquitylase for de-polyubiquitylation and stabilization of PTEN is less defined. We recently report that OTUD3 （OTU domain-containing protein 3） acts as a deubiquitylase for PTEN, de-polyubiquitylates and stabilizes PTEN, then functions as a tumor suppressor in the regulation of breast cancer development. This progress revealed a molecular mechanism that stabilizes PTEN by antagonizing its ubiquitylation.

关 键 词：PTEN 去泛素化酶 OTUD3 乳腺癌 

分 类 号：R730.2[医药卫生—肿瘤]