Gastric Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 15, 2004; 10(2): 161-166
Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.161
Effect of staurosporine on cycle human gastric cancer cell
Min-Wen Ha, Ke-Zuo Hou, Yun-Peng Liu, Yuan Yuan
Min-Wen Ha, Yuan Yuan, Cancer Institute of the First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
Ke-Zuo Hou, Yun-Peng Liu, Department of Oncology of the First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China
Author contributions: All authors contributed equally to the work.
Supported by The China State Key Basic Research Program, No. G1998051203
Correspondence to: Professor Yuan Yuan, Cancer Institute of the First Affiliated Hospital of China Medical University, 155 Northern Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, China. yyuan@mail.cmu.edu.cn
Telephone: +86-24-23256666 Fax: +86-24-22703576
Received: June 5, 2003
Revised: July 17, 2003
Accepted: July 24, 2003
Published online: January 15, 2004
Abstract

AIM: To study the effect of staurosporine (ST) on the cell cycle of human gastric cancer cell lines MGC803 and SGC7901.

METHODS: Cell proliferation was evaluated by trypan blue dye exclusion method. Apoptotic morphology was observed under a transmission electron microscope. Changes of cell cycle and apoptotic peaks of cells were determined by flow cytometry. Expression of P21WAF1 gene was examined using immunohistochemistry and RT-PCR.

RESULTS: The growth of MGC803 and SGC7901 cells was inhibited by ST. The inhibitory concentrations against 50% cells (IC50) at 24 h and 48 h were 54 ng/ml and 23 ng/ml for MGC803, and 61 ng/ml and 37 ng/ml for SGC7901. Typical apoptotic bodies and apoptotic peaks were observed 24 h after cells were treated wth ST at a concentration of 200 ng/ml. The percentage of cells at G0/G1 phase was decreased and that of cells at G2/M was increased significantly in the group treated wth ST at the concentrations of 40 ng/ml, 60 ng/ml, 100 ng/ml for 24 h, compared with the control group (P < 0.01). The expression levels of P21WAF1 gene in both MGC803 and SGC7901 cells were markedly up-regulated after treatment with ST.

CONCLUSION: ST can cause arrest of gastric cancer cells at G2/M phase, which may be one of the mechanisms that inhibit cell proliferation and cause apoptosis in these cells. Effect of ST on cells at G2/M phase may be attributed to the up-regulattion of P21WAF1 gene.

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