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Effect of Helicobacter pylori infection on expression of Bcl-2 family members in gastric adenocarcinoma

机译:幽门螺杆菌感染对胃腺癌Bcl-2家族成员表达的影响

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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 resect/on margin tissues (Bid vs Bcl-2, r=0331, 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.
机译:目的:探讨幽门螺杆菌感染对胃腺癌Bcl-2家族成员表达的影响。方法:对95例胃腺癌及切缘组织进行了研究。半定量RT-PCR用于测量Bid,Bax和Bcl-2 mRNA表达。结果:未感染幽门螺杆菌,cagA〜-H幽门螺杆菌感染和cagA〜+ H幽门螺杆菌感染的胃腺癌组织中Bid和Bax的表达依次升高(Bid,0.304、0.422和0.855,P <0.05;分别为0.309、0.650和0.979,P <0.05)。与未感染幽门螺杆菌的胃癌相比,感染cagA〜-H幽门螺杆菌和cagA〜+ H幽门螺杆菌的胃腺癌组织中Bcl-2 mRNA的水平显着升高(0.696和0.849 vs 0.411,P <0.05)。 Bid,Bax和Bcl-2在无幽门螺杆菌感染,cagA〜-幽门螺杆菌感染和cagA〜+幽门螺杆菌感染的切除边缘组织中的表达依次升高(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、0.371、0.487和0.619,P <0.05)。在幽门螺杆菌阴性样本中,腺癌组织中Bid和Bax的表达分别与Bcl-2呈负相关(Bid vs Bcl-2,r = -0.409,P <0.05; Bax vs Bcl-2,r = -0.451, P <0.05)。在幽门螺杆菌阳性标本中,Bid和Bax在腺癌组织中的表达与Bcl-2不相关(Bid vs Bcl-2,r = 0.187,P> 0.05; Bax vs Bcl-2,r = 0.201,P> 0.05),但在切除/上缘组织中分别与Bcl-2呈正相关(Bid vs Bcl-2,r = 0331,P <0.05; Bax vs Bcl-2,r = 0.295,P <0.05)。结论幽门螺杆菌可能会提高Bid,Bax和Bcl-2 mRNA的表达水平,并导致这些凋亡相关基因的表达失调,这可能在幽门螺杆菌诱发的胃腺癌发生过程中发挥作用。

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