Cell Death Differ:USP39和TRIM26通过拮抗介导ZEB1泛素化水平影响肝细胞癌的发生发展

2021-03-05 xiaozeng MedSci原创

肝细胞癌(HCC)是一种具有高发病率和高死亡率的恶性肿瘤。

肝细胞癌(HCC)是一种具有高发病率和高死亡率的恶性肿瘤。仅在2018年里,共1810万例癌症病例中有841,080例HCC患者,且在960万例癌症死亡病例中占了781,631例。疾病的术后复发和转移是HCC患者预后改善的一大障碍,患者的总体5年生存率较低。

既往研究显示,HCC的发生发展与异常的上皮-间充质转化(EMT)进程相关,后者会诱导细胞迁移作用并使肿瘤细胞扩散。泛素-蛋白酶体系统(UPS)泛素化和去泛素化修饰之间的协调是重要的翻译后调节机制,其能够负责EMT相关蛋白的降解和更新。

越来越多的证据表明,去泛素化酶USP39在HCC的发生发展中起着至关重要的作用。然而,其相关的分子机制尚未清楚。

USP39在人HCC组织中高表达且与患者的不良预后相关

在该研究中,研究人员发现USP39在人HCC组织中高表达,且与患者的不良预后相关。此外,敲除USP39能够通过促进ZEB1的降解来抑制HCC细胞的增殖和转移。

USP39和TRIM26在体内发挥拮抗作用并促进HCC的发展

有趣的是,免疫共沉淀和免疫荧光染色实验显示,USP39与TRIM26直接相互作用。进一步的研究显示,在人HCC组织中TRIM26低表达,且会抑制HCC细胞的增殖和迁移。在HCC中,TRIM26能够通过泛素化作用促进ZEB1蛋白的降解。研究人员发现,USP39与TRIM26是以拮抗模式而非竞争模式来行使作用,且通过调控ZEB1的稳定性来影响HCC的发生发展。


总而言之,该研究结果揭示了USP39和TRIM26调控ZEB1泛素化水平并影响HCC细胞增殖和迁移的新机制。研究人员表明,在高ZEB1蛋白水平的HCC病例中,通过恢复TRIM26或抑制USP39表达的靶向治疗新策略或能够抑制HCC的发生发展。


原始出处:

Li, X., Yuan, J., Song, C. et al. Deubiquitinase USP39 and E3 ligase TRIM26 balance the level of ZEB1 ubiquitination and thereby determine the progression of hepatocellular carcinoma. Cell Death Differ (01 March 2021).

 

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    2021-12-14 维他命
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    2021-07-02 xjy02
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    2021-03-07 cy0328

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