Published online Mar 14, 2015. doi: 10.3748/wjg.v21.i10.3055
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
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.
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.