Brief Reports
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2004; 10(18): 2731-2734
Published online Sep 15, 2004. doi: 10.3748/wjg.v10.i18.2731
Diallyl disulfide-induced G2/M arrest of human gastric cancer MGC803 cells involves activation of p38 MAP kinase pathways
Jing-Ping Yuan, Gui-Hua Wang, Hui Ling, Qi Su, Yue-Hong Yang, Ying Song, Rong-Jun Tang, Yao Liu, Chen Huang
Jing-Ping Yuan, Gui-Hua Wang, Yue-Hong Yang, Department of Pathology, Central Hospital of Wuhan, Wuhan 430014, Hubei Province, China
Hui Ling, Qi Su, Ying Song, Rong-Jun Tang, Yao Liu, Chen Huang, Institute of Oncology, Medical College, Nanhua University, Hengyang 421001, Hunan Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Natural Science Foundation of Hunan Province, No. 02JJY2026, 01JJY2146 and the Foundation of Hunan Province Education Department, No. 01A016
Correspondence to: Professor Qi Su, Institute of Oncology, Nanhua University, Hengyang 421001, Hunan Province, China. suqi1@hotmail.com
Telephone: +86-734-8281547 Fax: +86-734-8281547
Received: April 2, 2003
Revised: April 23, 2003
Accepted: May 21, 2003
Published online: September 15, 2004
Abstract

AIM: To determine the role of p38 MAP kinase signal transduction pathways in diallyl disulfide (DADS)-induced G2/M arrest in human gastric cancer MGC803 cells.

METHODS: MGC803 cell growth inhibition was measured by MTT assay. Phase distribution of cell cycle was analyzed by flow cytometry. Expression of Cdc25C, p38, phosphorylation of p38 (pp38) were determined by Western blotting.

RESULTS: MTT assay showed that SB203580, a specific p38 MAPK inhibitor blocked DADS-induced growth inhibition. Flow cytometry analysis revealed that treatment of MGC803 cells with 30 mg/L DADS increased the percentage of cells in the G2/M phase from 9.3% to 39.4% (P < 0.05), whereas inhibition of p38 activity by SB203580 abolished induction of G2/M arrest by DADS. Western blotting showed that phosphorylation of p38 was increased 3.52-fold following treatment of MGC803 cells with 30 mg/L DADS for 20 min (P < 0.05), whereas Cdc25C was decreased 68% following treatment of MGC803 cells with 30 mg/L DADS for 24 h (P < 0.05). Decreased Cdc25C protein expression by DADS was attenuated by SB203580 (P < 0.05).

CONCLUSION: DADS-induced G2/M arrest of MGC803 cells involves activation of p38 MAP kinase pathways. Decreased Cdc25C protein expression by p38 MAPK played a crucial role in G2/M arrest after treatment with DADS.

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