Liver Cancer
Copyright ©2005 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jan 14, 2005; 11(2): 204-207
Published online Jan 14, 2005. doi: 10.3748/wjg.v11.i2.204
Specific COX-2 inhibitor NS398 induces apoptosis in human liver cancer cell line HepG2 through BCL-2
Dong-Sheng Huang, Ke-Zhen Shen, Jian-Feng Wei, Ting-Bo Liang, Shu-Sen Zheng, Hai-Yang Xie
Dong-Sheng Huang, Ke-Zhen Shen, Jian-Feng Wei, Ting-Bo Liang, Shu-Sen Zheng, Hai-Yang Xie, Department of Hepatobiliary Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou 310003, Zhejiang Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Hai-Yang Xie, Department of Hepatobiliary Pancreatic Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province,China. xiehaiyang@zju.edu.cn
Telephone: +86-571-87236570 Fax: +86-571-87236570
Received: June 21, 2003
Revised: June 23, 2003
Accepted: September 25, 2003
Published online: January 14, 2005
Abstract

AIM: To evaluate the effects of NS-398, a cyclooxygenase-2 (COX-2) inhibitor, on the proliferation and apoptosis of HepG2 cells.

METHODS: The effects of NS-398 on the proliferation of HepG2 cells were evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells. DNA ploidy and apoptotic cell percentage were calculated by flow cytometry. The expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. Furthermore, expression level of Bcl-2 was detected using Western blot in HepG2 after treated with NS-398.

RESULTS: NS-398 inhibited cell proliferation and induced apoptosis of HepG2 cells in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with increase of NS-398 concentration. The quiescent G0/G1 phase was accumulated with decrease of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, and no correlations were found between COX-2 mRNA and HepG2 cell proliferation and apoptosis induced by NS-398 (r = 0.056 and r = 0.119, respectively). Bcl-2 protein level was inhibited after treated with NS-398.

CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis of HepG2 cells. Mechanisms involved may be accumulation of quiescent G0/G1 phase and decrease of Bcl-2 expression.

Keywords: Liver cancer; NS-398; Bcl-2 protein; COX-2