Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.227
Revised: August 9, 2003
Accepted: August 16, 2003
Published online: January 15, 2004
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.