Basic Study
Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 21, 2019; 25(43): 6386-6403
Published online Nov 21, 2019. doi: 10.3748/wjg.v25.i43.6386
Ubiquitin-conjugating enzyme E2T knockdown suppresses hepatocellular tumorigenesis via inducing cell cycle arrest and apoptosis
Jian Guo, Mu Wang, Jun-Ping Wang, Chang-Xin Wu
Jian Guo, Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Institute of Biotechnology, Shanxi University, Taiyuan 030006, Shanxi Province, China
Jian Guo, Department of General Surgery, Shanxi Provincial People’s Hospital, the Affiliated People’s Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China
Mu Wang, Department of Neurology, Shanxi Provincial People’s Hospital, the Affiliated People’s Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China
Jun-Ping Wang, Department of Gastroenterology, Shanxi Provincial People’s Hospital, the Affiliated People’s Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi Province, China
Chang-Xin Wu, The Institutes of Biomedical Sciences, Shanxi University, Taiyuan 03006, Shanxi Province, China
Chang-Xin Wu, Key Laboratory of Molecular Biology and Biochemistry of Ministry of Education, Shanxi University, Taiyuan 030006, Shanxi Province, China
Author contributions: Wu CX designed the research; Guo J performed the majority of experiments and wrote the paper; Wang JP and Wang M coordinated the research.
Institutional review board statement: This study was approved by the ethics committee of The Affiliated People's Hospital of Shanxi Medical University.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of The Affiliated People's Hospital of Shanxi Medical University (IACUC protocol number: 20171236).
Conflict-of-interest statement: No potential conflicts of interest are disclosed.
Data sharing statement: Data are available from the first author at guo10121012@163.com
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Chang-Xin Wu, PhD, Professor, The Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, Shanxi Province, China. cxw20@sxu.edu.cn
Telephone: +86-351-4960141 Fax: +86-351-4960123
Received: January 16, 2019
Peer-review started: January 16, 2019
First decision: February 13, 2019
Revised: September 10, 2019
Accepted: September 13, 2019
Article in press: September 13, 2019
Published online: November 21, 2019
Core Tip

Core tip: Ubiquitin-conjugating enzyme E2T (UBE2T) is a member of the ubiquitin-proteasome family. Although it has been reported that UBE2T promotes the growth of hepatocellular carcinoma (HCC) cells, the role of UBE2T in the HCC cell cycle, apoptosis, and tumorigenesis is unclear. UBE2T was highly expressed in HCC tissues, and its expression was correlated with the survival of HCC patients. Silencing of UBE2T reduced the viability and xenograft tumor growth of HCC cells. Additionally, cell cycle arrest and apoptosis were induced by UBE2T knockdown. Numerous genes were regulated by UBE2T silencing in HCC cells. Therefore, UBE2T is a novel diagnostic and therapeutic target for HCC.