The multifaceted role of E3 ubiquitin ligases in cancer metastasis: mechanisms, targets, and therapeutic implications

E3泛素连接酶在癌症转移中的多重作用:机制、靶点和治疗意义

阅读:4

Abstract

Cancer metastasis is one of the hallmarks of cancer. This multistep process involves a cascade of alterations at the cellular and molecular level, including the epithelial-to-mesenchymal transition (EMT), invasion, migration, extracellular matrix (ECM) degradation, angiogenesis, and colonization. Expression level of critical factors associated with these processes is altered at the post-translational level through ubiquitination. Therefore, E3 ubiquitin ligases, components of the ubiquitin-mediated proteasome system, play a crucial role in controlling each step of metastasis by promoting the ubiquitination of several important factors. In this review, we have summarized the importance of E3 ligase in metastasis. Several E3 ligases act as promoters, while others act as repressors of metastasis. This article focuses on the potential role of E3 ubiquitin ligases in cancer metastasis and reveals their molecular function and targets, which are crucial for therapeutic interventions in anti-cancer therapies. Further, we covered the development of small molecule inhibitors and proteolysis-targeting chimeras to target E3 ubiquitin ligases involved in promoting metastasis for therapeutic intervention. Despite tremendous advancements, there are still many unanswered questions, especially regarding the complete characterization of the diverse range of E3 ligase functions and the conversion of preclinical discoveries into successful clinical treatments. In addition, future directions are concentrated on using technologies to develop highly specific therapeutic interventions and exploring their potential in combination with other treatment modalities, including immunotherapy, to ultimately overcome the challenges of cancer metastasis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。