Effect of<i>Helicobacter pylori</i>infection on expressions of Bcl-2 family members in gastric adenocarcinoma

Zhang, Hao; Fang, Dian‐Chun; Wang, Rongquan; Yang, Shi‐Ming; Liu, Haifeng; Luo, Yang

doi:10.3748/wjg.v10.i2.227

Cited by 27 publications

(29 citation statements)

References 46 publications

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“…Bcl-2 regulates apoptotic processes, and can lead to apoptotic resistance when highly expressed. This protein has been shown to be up-regulated during H. pylori infection with cag ϩ strains (52) and H. pylori-associated gastric cancers (38,39). In this study, Bcl-2 levels were expressed at much higher levels in GECs with wild-type strains than with CagA-deficient strains.…”

Section: Discussionmentioning

confidence: 57%

“…Because Bcl-2 expression is up-regulated during H. pylori infection and gastric atrophy and cancer (38,39), and down-regulated in apoptotic cells (40), the expression of Bcl-2 was investigated during infection with H. pylori and upon pretreatment with rMIF. Flow cytometric analysis revealed that Bcl-2 expression is induced in GECs upon exposure to H. pylori, but is decreased when cells were exposed to CagA-deficient strains in comparison to wild-type strains (Fig.…”

Section: H Pylori-induced Mif Induces Bcl-2 Expressionmentioning

confidence: 99%

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Helicobacter pyloriCagA-Dependent Macrophage Migration Inhibitory Factor Produced by Gastric Epithelial Cells Binds to CD74 and Stimulates Procarcinogenic Events

Beswick

Pinchuk

Suárez

et al. 2006

The Journal of Immunology

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Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that has recently been implicated in carcinogenesis. Helicobacter pylori, which is closely linked to gastric cancer, induces the gastric epithelium to produce proinflammatory cytokines, including MIF. MIF can bind to CD74, which we have previously shown to be highly expressed on the surface of gastric epithelial cells (GEC) during H. pylori infection. In this study, we sought to investigate the role of the H. pylori-induced MIF on epithelial proliferation and procarcinogenic events. Upon establishing a role for the H. pylori CagA virulence factor in MIF production, MIF binding to CD74 on GEC was confirmed. rMIF and H. pylori were shown to increase GEC proliferation, which was decreased when cagA− strains were used and when CD74 was blocked by mAbs. Apoptosis was also decreased by MIF, but increased by cagA− strains that induced much lower amounts of MIF than the wild-type bacteria. Furthermore, MIF binding to CD74 was also shown to decrease p53 phosphorylation and up-regulate Bcl-2 expression. This data describes a novel system in which an H. pylori virulence factor contributes to the production of a host factor that in turn up-regulates procarcinogenic events by the gastric epithelium.

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Section: Discussionmentioning

confidence: 57%

Section: H Pylori-induced Mif Induces Bcl-2 Expressionmentioning

confidence: 99%

Helicobacter pyloriCagA-Dependent Macrophage Migration Inhibitory Factor Produced by Gastric Epithelial Cells Binds to CD74 and Stimulates Procarcinogenic Events

Beswick

Pinchuk

Suárez

et al. 2006

The Journal of Immunology

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“…The biological significance between H pylori and c-Myc is still not understood. A study from Zang et al [38] has linked the c-Myc expression with cell proliferation while a study from Yang et al [40] on a gastric carcinoma cell line has pointed to a relationship with apoptosis. On the other hand, Kim et al [42] have shown a decrease of c-Myc expression after H pylori eradication, but not in its mRNA level, showing the complexity of this process.…”

Section: Discussionmentioning

confidence: 99%

“…In present study, the expression of c-Myc was higher in the g roups without EBV infection indicating a relationship of c-Myc with gastric carcinogenesis but not with EBV infection [41] . Additionally, some studies point to the involvement of H pylori with c-Myc [38,41] . The biological significance between H pylori and c-Myc is still not understood.…”

Section: Discussionmentioning

confidence: 99%

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H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

Lima

Lima²,

André³

et al. 2008

WJG

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AIM: To investigate the interrelationship betweenH pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression.METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS:The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P = 0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori .However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION:The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.

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The correlations between the expression of FGFR4 protein and clinicopathological parameters as well as prognosis of gastric cancer patients

Zhang

Zhou

et al. 2012

Journal of Surgical Oncology

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Effect ofHelicobacter pyloriinfection on expressions of Bcl-2 family members in gastric adenocarcinoma

Cited by 27 publications

References 46 publications

Helicobacter pyloriCagA-Dependent Macrophage Migration Inhibitory Factor Produced by Gastric Epithelial Cells Binds to CD74 and Stimulates Procarcinogenic Events

Helicobacter pyloriCagA-Dependent Macrophage Migration Inhibitory Factor Produced by Gastric Epithelial Cells Binds to CD74 and Stimulates Procarcinogenic Events

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression

The correlations between the expression of FGFR4 protein and clinicopathological parameters as well as prognosis of gastric cancer patients

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