H Pylori
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 15, 2004; 10(2): 227-230
Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.227
Effect of Helicobacter pylori infection on expressions of Bcl-2 family members in gastric adenocarcinoma
Hao Zhang, Dian-Chun Fang, Rong-Quan Wang, Shi-Ming Yang, Hai-Feng Liu, Yuan-Hui Luo
Hao Zhang, Dian-Chun Fang, Rong-Quan Wang, Shi-Ming Yang, Hai-Feng Liu, Yuan-Hui Luo, Department of Gastroenterology of Southwest Hospital, Third Military Medical University, Chongqing 400038, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No.30070043, and the Key Programs of the Military Medical and Health Foundation during the 10th Five-Year Plan Period, No.01Z075
Correspondence to: Professor Dian-Chun Fang, Department of Gastroenterology of Southwest Hospital, Chongqing 400038, China. fangdianchun@hotmail.com
Telephone: +86-23-68754124
Received: July 12, 2003
Revised: August 9, 2003
Accepted: August 16, 2003
Published online: January 15, 2004
Abstract

AIM: To investigate the effect of Helicobacter pylori (H pylori) infection on the expressions of Bcl-2 family members in gastric adenocarcinoma.

METHODS: Gastric adenocarcinoma and resection margin tissues of 95 patients were studied. Semi-quantitative RT-PCR was used to measure Bid, Bax and Bcl-2 mRNA expressions.

RESULTS: Expressions of Bid and Bax in gastric adenocarcinoma tissues without H pylori infection, with cagA-H pylori infection and cagA+H pylori infection increased significantly in turn (Bid, 0.304, 0.422 and 0.855 respectively, P < 0.05; Bax, 0.309, 0.650 and 0.979 respectively, P < 0.05). Bcl-2 mRNA levels increased significantly in gastric adenocarcinoma tissues with cagA-H pylori infection and cagA+H pylori infection, compared with those without H pylori infection (0.696 and 0.849 vs 0.411, P < 0.05). Expressions of Bid, Bax and Bcl-2 in resection margin tissues without H pylori infection, with cagA-H pylori infection and cagA+H pylori infection increased significantly in turn (Bid, 0.377, 0.686 and 0.939 respectively, P < 0.05; Bax, 0.353, 0.645 and 1.001 respectively, P < 0.05; Bcl-2, 0.371, 0.487 and 0.619 respectively, P < 0.05). In H pylori negative specimens, expressions of Bid and Bax correlated negatively with that of Bcl-2 respectively in adenocarcinoma tissues (Bid vs Bcl-2, r = -0.409, P < 0.05; Bax vs Bcl-2, r = -0.451, P < 0.05). In H pylori positive specimens, expressions of Bid and Bax did not correlate with that of Bcl-2 in adenocarcinoma tissues (Bid vs Bcl-2, r = 0.187, P > 0.05; Bax vs Bcl-2, r = 0.201, P > 0.05), but correlated positively with that of Bcl-2 respectively in resection margin tissues (Bid vs Bcl-2, r = 0.331, P < 0.05; Bax vs Bcl-2, r = 0.295, P < 0.05).

CONCLUSION: H pylori may enhance Bid, Bax and Bcl-2 mRNA levels and cause deregulation of these apoptosis-associated genes expressions, which may play a role during development of gastric adenocarcinoma induced by H pylori.

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