文章：

SMURF1：肿瘤细胞进展的启动子？

SMURF1, a promoter of tumor cell progression? 

原文发布日期：2020-11-17 

英文摘要：

Overexpression of HECT-type E3 ubiquitin ligase SMURF1 is correlated with poor prognosis in patients with various cancers, such as glioblastoma, colon cancer, and clear cell renal cell carcinoma. SMURF1 acts as a tumor promoter by ubiquitination modification and/or degradation of tumor-suppressing proteins. Combined treatment of Smurf1 knockdown with rapamycin showed collaborative antitumor effects in mice. This review described the role of HECT, WW, and C2 domains in regulating SMURF1 substrate selection. We summarized up to date SMURF1 substrates regulating different type cell signaling, thus, accelerating tumor progression, invasion, and metastasis. Furthermore, the downregulation of SMURF1 expression, inhibition of its E3 activity and regulation of its specificity to substrates prevent tumor progression. The potential application of SMURF1 regulators, specifically, wisely choose certain drugs by blocking SMURF1 selectivity in tumor suppressors, to develop novel anticancer treatments. 

摘要翻译： 

HECT型E3泛素连接酶SMURF1的过表达与胶质母细胞瘤、结肠癌和透明细胞肾细胞癌等多种癌症患者的不良预后相关。SMURF1通过泛素化修饰和/或降解抑癌蛋白发挥肿瘤促进作用。在小鼠实验中，联合使用Smurf1基因敲除与雷帕霉素治疗显示出协同抗肿瘤效果。本综述阐述了HECT结构域、WW结构域和C2结构域在调控SMURF1底物选择中的作用，系统总结了SMURF1通过调控不同细胞信号通路底物促进肿瘤进展、侵袭和转移的最新研究成果。此外，下调SMURF1表达、抑制其E3活性及调控底物特异性可有效阻止肿瘤进展。通过特异性阻断SMURF1对抑癌蛋白的选择性，合理选用靶向药物调控SMURF1活性，有望为开发新型抗癌治疗方案提供潜在策略。

原文链接：

SMURF1, a promoter of tumor cell progression?