Zhang Hao, Fang Dian-Chun, Wang Rong-Quan, Yang Shi-Ming, Liu Hai-Feng, Luo Yuan-Hui
Department of Gastroenterology of Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
World J Gastroenterol. 2004 Jan 15;10(2):227-30. doi: 10.3748/wjg.v10.i2.227.
To investigate the effect of Helicobacter pylori (H pylori) infection on the expressions of Bcl-2 family members in gastric adenocarcinoma.
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.
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).
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.
探讨幽门螺杆菌(H pylori)感染对胃腺癌中Bcl-2家族成员表达的影响。
对95例患者的胃腺癌及手术切缘组织进行研究。采用半定量逆转录聚合酶链反应(RT-PCR)检测Bid、Bax和Bcl-2 mRNA表达。
未感染H pylori、cagA- H pylori感染及cagA+ H pylori感染的胃腺癌组织中,Bid和Bax的表达依次显著升高(Bid分别为0.304、0.422和0.855,P<0.05;Bax分别为0.309、0.650和0.979,P<0.05)。与未感染H pylori的胃腺癌组织相比,cagA- H pylori感染及cagA+ H pylori感染的胃腺癌组织中Bcl-2 mRNA水平显著升高(分别为0.696和0.849,对比0.411,P<0.05)。未感染H pylori、cagA- H pylori感染及cagA+ H pylori感染的手术切缘组织中,Bid、Bax和Bcl-2的表达依次显著升高(Bid分别为0.377、0.686和0.939,P<0.05;Bax分别为0.353、0.645和1.001,P<0.05;Bcl-2分别为0.371、0.487和0.619,P<0.05)。在H pylori阴性标本中,胃腺癌组织中Bid和Bax的表达分别与Bcl-2呈负相关(Bid与Bcl-2,r=-0.409,P<0.05;Bax与Bcl-2,r=-0.451,P<0.05)。在H pylori阳性标本中,胃腺癌组织中Bid和Bax的表达与Bcl-2无相关性(Bid与Bcl-2,r=0.187,P>0.05;Bax与Bcl-2,r=0.201,P>0.05),但在手术切缘组织中分别与Bcl-2呈正相关(Bid与Bcl-2,r=0.331,P<0.05;Bax与Bcl-2,r=0.295,P<0.05)。
H pylori可能增强Bid、Bax和Bcl-2 mRNA水平,导致这些凋亡相关基因表达失调,这可能在H pylori诱导的胃腺癌发生过程中起作用。