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Expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa.三叶因子2表达及幽门螺杆菌感染在胃黏膜癌变中的作用
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2
Overexpression of c-fos in Helicobacter pylori-induced gastric precancerosis of Mongolian gerbil.c-fos在幽门螺杆菌诱导的蒙古沙鼠胃癌前病变中的过表达。
World J Gastroenterol. 2003 Mar;9(3):521-4. doi: 10.3748/wjg.v9.i3.521.
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Association of cyclooxygenase-2 expression with Hp-cagA infection in gastric cancer.环氧化酶-2表达与胃癌中幽门螺杆菌细胞毒素相关基因A感染的相关性
World J Gastroenterol. 2003 Feb;9(2):246-9. doi: 10.3748/wjg.v9.i2.246.
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Helicobacter pylori infection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation.幽门螺杆菌感染通过p53-Rb肿瘤抑制系统突变和端粒酶重新激活引发胃癌。
World J Gastroenterol. 2003 Jan;9(1):54-8. doi: 10.3748/wjg.v9.i1.54.
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Helicobacter pylori infection and gastric cancer: evidence from a retrospective cohort study and nested case-control study in China.幽门螺杆菌感染与胃癌：来自中国一项回顾性队列研究和巢式病例对照研究的证据
World J Gastroenterol. 2002 Dec;8(6):1103-7. doi: 10.3748/wjg.v8.i6.1103.
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Peptides derived from BH3 domains of Bcl-2 family members: a comparative analysis of inhibition of Bcl-2, Bcl-x(L) and Bax oligomerization, induction of cytochrome c release, and activation of cell death.源自Bcl-2家族成员BH3结构域的肽：对Bcl-2、Bcl-x(L)和Bax寡聚化抑制、细胞色素c释放诱导及细胞死亡激活的比较分析
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Lens epithelial cell death and reduction of anti-apoptotic protein Bcl-2 in human anterior polar cataracts.人前极性白内障中晶状体上皮细胞死亡及抗凋亡蛋白Bcl-2减少
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[Relation between Helicobacter pylori and diseases: knowledge for clinician].[幽门螺杆菌与疾病的关系：临床医生须知]
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幽门螺杆菌感染对胃腺癌中Bcl-2家族成员表达的影响。

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

作者信息

Zhang Hao, Fang Dian-Chun, Wang Rong-Quan, Yang Shi-Ming, Liu Hai-Feng, Luo Yuan-Hui

机构信息

Department of Gastroenterology of Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

出版信息

World J Gastroenterol. 2004 Jan 15;10(2):227-30. doi: 10.3748/wjg.v10.i2.227.

DOI:10.3748/wjg.v10.i2.227
PMID:14716828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4717009/
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.

摘要

目的

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。

方法

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。

结果

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）。

结论

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。