Ubiquitin-like protein FAT10 promotes bladder cancer progression by stabilizing survivin.
Ubiquitin-like protein FAT10 promotes bladder cancer progression by stabilizing survivin.
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泛素样蛋白 FAT10 通过稳定生存素促进膀胱癌进展。
DOI：
10.18632/oncotarget.12976
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发表时间：
2016-12-06
期刊：
影响因子：
--
通讯作者：
Shao J
中科院分区：
文献类型：
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作者：
Dong D;Jiang W;Lei J;Chen L;Liu X;Ge J;Che B;Xi X;Shao J
人类HLA-F邻近转录物10 （FAT10）是泛素样修饰蛋白家族的成员，与癌症的发展有关。此外，Survivin蛋白促进膀胱癌（BC）的增殖。在这项研究中，我们探索了FAT10和Survivin之间的联系。FAT10表达在BC组织样本中显著上调，Kaplan-Meier生存分析显示，FAT10高表达的BC患者的总生存期比FAT10低表达的患者短。此外，rnai介导的FAT10敲低降低了Survivin蛋白水平，抑制了体外和体内BC的增殖。FAT10直接结合并稳定Survivin蛋白，通过抑制泛素介导的降解促进癌细胞增殖。这些结果揭示了FAT10通过直接稳定BC中Survivin蛋白促进肿瘤增殖的新机制。
Human HLA-F adjacent transcript 10 (FAT10) is a member of the ubiquitin-like-modifier family of proteins, which have been implicated in cancer development. In addition, the Survivin protein promotes proliferation in bladder cancer (BC). In this study, we explored the link between FAT10 and Survivin. FAT10 expression was dramatically up-regulated in BC tissue samples, and Kaplan-Meier survival analysis revealed that BC patients with high FAT10 expression had shorter overall survival than those with low FAT10 expression. Moreover, RNAi-mediated FAT10 knockdown decreased Survivin protein levels and inhibited BC proliferation both in vitro and in vivo. FAT10 directly bound to and stabilized Survivin protein, thereby promoting cancer cell proliferation by inhibiting ubiquitin-mediated degradation. These results reveal a novel mechanism by which FAT10 promotes tumor proliferation by directly stabilizing Survivin protein in BC.