中文摘要：

PTEN（phosphatase and tension homology,deleted in chromosome10）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 protein3）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。

英文摘要：

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.