Evidence-Based Medicine
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 14, 2015; 21(10): 3055-3065
Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.3055
Decaprenyl diphosphate synthase subunit 2 as a prognosis factor in hepatocellular carcinoma
Wei Huang, Fei Gao, Kang Li, Wen Wang, Ya-Rou Lai, Shao-Hui Tang, Dong-Hua Yang
Wei Huang, Fei Gao, Wen Wang, Ya-Rou Lai, Shao-Hui Tang, Dong-Hua Yang, Department of Gastroenterology, The First Affiliated Hospital of Jinan University, Guangzhou 510630, Guangdong Province, China
Kang Li, Department of Gastroenterology, Panyu Hexian Memorial Hospital, Guangzhou 510630, Guangdong Province, China
Author contributions: Huang W and Gao F performed experiments and contributed equally to this work; Wang W and Tang SH collected tissue samples; Lai YR and Li K conducted statistical analyses; Huang W and Yang DH conceived experiments and analyzed data; all authors were involved in writing the paper and final approval of the submitted and published versions.
Supported by Funding from the Fundamental Research Funds for the First Clinical College of Jinan University, No. 2014110; the National Natural Science Foundation of China, No. 81401973; the Fundamental Research Funds for the Central Universities of China, No. 21614304; and the Medical Scientific Research Foundation of Guangdong Province of China, No. B2014222.
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/
Correspondence to: Wei Huang, Professor, Department of Gastroenterology, the First Affiliated Hospital of Jinan University, 613 West Huangpu Road, Guangdong Province, Guangzhou 510630, China. thuangw@163.com
Telephone: +86-20-38688622 Fax: +86-20-38688622
Received: July 12, 2014
Peer-review started: July 12, 2014
First decision: August 15, 2014
Revised: August 21, 2014
Accepted: October 20, 2014
Article in press: October 21, 2014
Published online: March 14, 2015
Processing time: 246 Days and 21.5 Hours
Abstract

AIM: To investigate the involvement of decaprenyl diphosphate synthase subunit 2 (PDSS2) in development and progression of human hepatocellular carcinoma (HCC).

METHODS: PDSS2 protein expression was examined in well- and poorly differentiated HCC tumor samples. The levels of PDSS2 expression were compared with clinical features and prognosis of HCC patients. The effects of PDSS2 on cell proliferation, cell cycle, apoptosis, cell migration, and invasion in HCC HepG2 cells were also investigated.

RESULTS: PDSS2 was downregulated in poorly differentiated cancer samples compared with well-differentiated tumor samples, and the expression level was markedly lower in HCC tissues than in histologically normal tissue adjacent to the cancer. Reduced protein expression was negatively associated with the status of HCC progression. In addition, overexpression of PDSS2 dramatically suppressed cell proliferation and colony formation, and induced apoptosis in HepG2 cells by inducing G1-phase cell-cycle arrest. The migration and invasion capabilities of HepG2 cells were significantly decreased following PDSS2 overexpression.

CONCLUSION: Decreased PDSS2 expression is an unfavorable prognostic factor for HCC, and PDSS2 has potent anticancer activity in HCC tissues and HepG2 cells.

Keywords: Decaprenyl diphosphate synthase subunit 2; Hepatocellular carcinoma; Tumor suppressor

Core tip: We found that decaprenyl diphosphate synthase subunit 2 (PDSS2) was frequently downregulated in primary hepatocellular carcinoma (HCC), and the level of expression was markedly lower in poorly differentiated cancer samples compared with well-differentiated tumor tissues. Furthermore, the expression of PDSS2 was inversely correlated with clinical stage. Overexpression of PDSS2 in HepG2 cells decreased cell proliferation and induced G1-phase cell cycle arrest and apoptosis in human HCC cells. Moreover, PDSS2 reduced epithelial-mesenchymal transition in HCC.