Research Papers:

Ubiquitin-like protein FAT10 promotes bladder cancer progression by stabilizing survivin

Dingxiang Dong, Weifan Jiang, Jun Lei, Leifeng Chen, Xiuxia Liu, Jin Ge, Ben Che, Xiaoqing Xi and Jianghua Shao _

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Oncotarget. 2016; 7:81463-81473. https://doi.org/10.18632/oncotarget.12976

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Dingxiang Dong1,3,*, Weifan Jiang2,*, Jun Lei1,*, Leifeng Chen1,3, Xiuxia Liu3, Jin Ge3, Ben Che1,3, Xiaoqing Xi2, Jianghua Shao1,3

1Department of General Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, 33000, China

2Department of Urology Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, 33000, China

3Jiangxi Province Key Laboratory of Molecular Medicine, Nanchang, 33000, China

*These authors have contributed equally to this work

Correspondence to:

Jianghua Shao, email: [email protected]

Keywords: bladder carcinoma, FAT10 protein, tumor promoter, stabilize, survivin protein

Received: September 06, 2016     Accepted: October 14, 2016     Published: October 28, 2016


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.

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