Research Papers:

Usp5 functions as an oncogene for stimulating tumorigenesis in hepatocellular carcinoma

Yi Liu, Wei-Mao Wang, Ying-fei Lu, Lu Feng, Li Li, Ming-zhu Pan, Yu Sun, Chun-wai Suen, Wei Guo, Jian-xin Pang, Jin-Fang Zhang and Wei-Ming Fu _

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Oncotarget. 2017; 8:50655-50664. https://doi.org/10.18632/oncotarget.16901

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Yi Liu1, Wei-Mao Wang2, Ying-Fei Lu3, Lu Feng3, Li Li1, Ming-Zhu Pan1, Yu Sun4, Chun-Wai Suen2, Wei Guo5, Jian-Xin Pang6, Jin-Fang Zhang2,3,7 and Wei-Ming Fu6,7

1Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical University, Zhanjiang, Guangdong, China

2School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China

3Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong, China

4Shenzhen Enhance Techology Co. Ltd., Shenzhen, Guangdong, China

5Shenzhen Ritzcon Biological Techology Co. Ltd., Shenzhen, Guangdong, China

6School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China

7Guangzhou Institute of Advanced Technology, Chinese Academy of Sciences, Guangzhou, Guangdong, China

Correspondence to:

Wei-Ming Fu, email: [email protected]

Jian-Xin Pang, email: [email protected]

Keywords: Usp5, epatocellular carcinoma, proliferation, migration, P14

Received: September 06, 2016     Accepted: March 28, 2017     Published: April 06, 2017


As deubiquitinases, several ubiquitin specific protease members have been reported to mediate tumorigenesis. Although ubiquitin specific protease 5 (Usp5) was previously demonstrated to suppress p53 transcriptional activity and DNA repair, its role in carcinogenesis remains elusive. In this study, we sought to define a novel role of Usp5 in tumorigenesis. It was found that Usp5 was significantly upregulated in hepatocellular carcinoma (HCC) cells and most clinical specimens. Further functional investigation also showed that Usp5 knockdown suppressed cell proliferation, migration, drug resistance and induced apoptosis; on the other hand, Usp5 overexpression promoted colony formation, migration, drug resistance and tumorigenesis. Additionally, the inactivated p14ARF-p53 signaling was observed in Usp5 overexpressed HCC cells, while this signaling was activated by Usp5 knockdown. Therefore, our data demonstrated that Usp5 contributed to hepatocarcinogenesis by acting as an oncogene, which provides new insights into the pathogenesis of HCC and explores a promising molecular target for HCC diagnosis and therapy.

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