USP10 通过去泛素化调节 Musashi-2 的稳定性，并促进结肠癌肿瘤增殖。
USP10 regulates Musashi-2 stability via deubiquitination and promotes tumour proliferation in colon cancer.
机构信息
Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China.
Department of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, China.
出版信息
FEBS Lett. 2019 Feb;593(4):406-413. doi: 10.1002/1873-3468.13323. Epub 2019 Jan 16.
Recent studies have demonstrated that ubiquitin-specific protease 10 (USP10) plays a catalytic role in tumour suppression mainly by deubiquitinating its target proteins to enhance their stabilities. However, we found that USP10 could interact with and regulate the expression of oncogenic factor Musashi-2 (MSI2). We investigated whether USP10 positively regulates the expression of MSI2 by deubiquitination and confirmed the type of polyubiquitin chain that is linked to MSI2. We also explored the role of USP10 in regulating the proliferation of colon cancer through different experiments. This study provides a completely new perspective in understanding the role of USP10 in deubiquitination. In the future, USP10 may serve as a target for colon cancer treatment.
最近的研究表明，泛素特异性蛋白酶 10（USP10）主要通过去泛素化其靶蛋白来增强它们的稳定性，从而发挥肿瘤抑制作用。然而，我们发现 USP10 可以与致癌因子 Musashi-2（MSI2）相互作用并调节其表达。我们研究了 USP10 是否通过去泛素化来正向调节 MSI2 的表达，并确认了与 MSI2 相连的多泛素链的类型。我们还通过不同的实验探索了 USP10 在调节结肠癌细胞增殖中的作用。这项研究为理解 USP10 在去泛素化中的作用提供了一个全新的视角。在未来，USP10 可能成为结肠癌治疗的靶点。
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