Kuang Linghan, Jiang Yunhui, Li Chenghua, Jiang Yongmei
Department of Laboratory Medicine, West China Second University Hospital, Sichuan University, Chengdu, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, China.
Front Cell Dev Biol. 2021 Oct 12;9:757493. doi: 10.3389/fcell.2021.757493. eCollection 2021.
WW domain-containing E3 ubiquitin protein ligase 1 (WWP1) is a member of C2-WW-HECT E3 ligase family. Although it may execute carcinostatic actions in some scenarios, WWP1 functions as an oncoprotein under most circumstances. Here, we comprehensively review reports on regulation of WWP1 and its roles in tumorigenesis. We summarize the WWP1-mediated ubiquitinations of diverse proteins and the signaling pathways they involved, as well as the mechanisms how they affect cancer formation and progression. According to our analysis of database, in combination with previous reports, we come to a conclusion that WWP1 expression is augmented in various cancers. Gene amplification, as well as expression regulation mediated by molecules such as non-coding RNAs, may account for the increased mRNA level of WWP1. Regulation of enzymatic activity is another important facet to upregulate WWP1-mediated ubiquitinations. Based on the published data, we conclude that WWP1 employs interactions between multiple domains to autoinhibit its polyubiquitination activity in a steady state. Association of some substrates can partially release certain autoinhibition-related domains and make WWP1 have a moderate activity of polyubiquitination. Some cancer-related mutations can fully disrupt the inhibitory interactions and make WWP1 hyperactive. High expression level or hyperactivation of WWP1 may abnormally enhance polyubiquitinations of some oncoproteins or tumor suppressors, such as ΔNp63α, PTEN and p27, and ultimately promote cell proliferation, survival, migration and invasion in tumorigenesis. Given the dysregulation and oncogenic functions of WWP1 in some cancer types, it is promising to explore some therapeutic inhibitors to tune down its activity.
含WW结构域的E3泛素蛋白连接酶1(WWP1)是C2-WW-HECT E3连接酶家族的成员。尽管在某些情况下它可能发挥抑癌作用,但在大多数情况下WWP1起着癌蛋白的作用。在此,我们全面综述了关于WWP1调控及其在肿瘤发生中作用的报道。我们总结了WWP1介导的多种蛋白质的泛素化作用及其涉及的信号通路,以及它们影响癌症形成和进展的机制。根据我们对数据库的分析,并结合先前的报道,我们得出结论:WWP1在各种癌症中表达增加。基因扩增以及由非编码RNA等分子介导的表达调控,可能是WWP1 mRNA水平升高的原因。酶活性的调节是上调WWP1介导的泛素化作用的另一个重要方面。基于已发表的数据,我们得出结论:WWP1利用多个结构域之间的相互作用在稳态下自动抑制其多聚泛素化活性。某些底物的结合可部分释放某些与自动抑制相关的结构域,使WWP1具有适度的多聚泛素化活性。一些与癌症相关的突变可完全破坏抑制性相互作用,使WWP1过度活跃。WWP1的高表达水平或过度激活可能异常增强某些癌蛋白或肿瘤抑制因子(如ΔNp63α、PTEN和p27)的多聚泛素化作用,并最终在肿瘤发生过程中促进细胞增殖、存活、迁移和侵袭。鉴于WWP1在某些癌症类型中的失调和致癌功能,探索一些治疗性抑制剂来降低其活性是有前景的。