Gastric Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2004; 10(18): 2628-2631
Published online Sep 15, 2004. doi: 10.3748/wjg.v10.i18.2628
Effects of mifepristone on proliferation of human gastric adenocarcinoma cell line SGC-7901 in vitro
Da-Qiang Li, Zhi-Biao Wang, Jin Bai, Jie Zhao, Yuan Wang, Kai Hu, Yong-Hong Du
Da-Qiang Li, Zhi-Biao Wang, Jin Bai, Jie Zhao, Yuan Wang, Kai Hu, Yong-Hong Du, State Key Laboratory of Ultrasound Engineering in Medicine, Chongqing Medical University, Chongqing 400016, China
Author contributions: All authors contributed equally to the work.
Supported by the National Key Research Project Foundation of China, No. 96-905-02-01, and the National Natural Science Foundation of China, No. 39630340
Correspondence to: Dr. Zhi-Biao Wang, State Key Laboratory of Ultrasound Engineering in Medicine, Chongqing Medical University PO Box 153, Chongqing 400016, China. wangzhibiao@netease.com
Telephone: +86-23-68485022 Fax: +86-23-68485023
Received: August 6, 2003
Revised: August 23, 2003
Accepted: December 6, 2003
Published online: September 15, 2004
Abstract

AIM: To explore the effects of mifepristone, a progesterone receptor (PR) antagonist, on the proliferation of human gastric adenocarcinoma cell line SGC-7901 in vitro and the possible mechanisms involved.

METHODS: In situ hybridization was used to detect the expression of PR mRNA in SGC-7901 cells. After treatment with various concentrations of mifepristone (2.5, 5, 10, 20 μmol/L) at various time intervals, the ultrastructural changes, cell proliferation, cell-cycle phase distribution, and the expression of caspase-3 and Bcl-XL were analyzed using transmission electron microscopy (TEM), tetrazolium blue(MTT) assay, 3H-TdR incorporation, flow cytometry, and reverse transcription-polymerase chain reaction (RT-PCR).

RESULTS: Mifepristone markedly induced apoptosis and inhibited cell proliferation of PR- positive SGC-7901 cells revealed by TEM, MTT assay and 3H-TdR incorporation, in a dose- and time-dependent manner. The inhibitory rate was increased from 8.98% to 51.29%. Flow cytometric analysis showed mifepristone dose-dependently decreased cells in S and G2/M phases, increased cells in G0/G1 phase, reduced the proliferative index from 57.75% to 22.83%. In addition, mifepristone up-regulated the expression of caspase-3, and down- regulated the Bcl-XL expression, dose-dependently.

CONCLUSION: Mifepristone effectively inhibited the proliferation of PR-positive human gastric adenocarcinoma cell line SGC-7901 in vitro through multiple mechanisms, and may be a beneficial agent against human adenocarcinoma.

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