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Global gene expression of chemical carcinogen (N-methyl-N-nitrosourea), Helicobacter pylori infection, and high-salt diet-treated mouse gastric mucosa

ABSTRACT: Helicobacter pylori (H. pylori) infection and excessive salt intake are known as important risk factors for stomach cancer in humans. However, interactions of these two factors with gene expression profiles during gastric carcinogenesis remain unclear. In this study, we established a mouse gastric tumor model combining a chemical carcinogen, H. pylori infection and a high-salt diet. The tumor incidence and multiplicity in N-methyl-N-nitrosourea-treated mice were significantly increased by combination of H. pylori with a high-salt diet. In addition, detailed examination indicated that excessive salt could regulate progression of gastric tumor. Global gene expression profiles in glandular stomach of the mouse model were investigated by cDNA microarray analysis, and 36 and 31 more than twofold up-regulated and down-regulated genes, respectively, were detected in the H. pylori-infection and high-salt diet combined group compared with the other groups. Quantitative RT-PCR confirmed significant over-expression of several candidate genes including Cd177, Reg3g, and Muc13. These results suggest that our mouse model combined with H. pylori infection and high-salt diet is useful for gene expression profiling in gastric carcinogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE29444 | GEO | 2011/05/25

SECONDARY ACCESSION(S): PRJNA141555

REPOSITORIES: GEO

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Project description:Background: Helicobacter pylori is an important human pathogen that infects the human gastric mucosa leading to chronic inflammation which is responsible for severe gastroduodenal diseases. The Outer Inflammatory Protein A (OipA) of H. pylori is an important virulence factor. However, the role of OipA in gastric cancer and ulcer development is still not well-established. Phase variation within a CT dinucleotide repeat motif of oipA switches its expression “on” and “off”. This study aims to elucidate the role of OipA in H. pylori infection using oipA “on” and “off” clinical strains and oipA deletion mutant. Methods: Proteomics analysis was performed on AGS human gastric epithelial cell line post-infection with oipA “on” and “off” H. pylori using liquid chromatography / mass spectrometry (LC/MS). In addition, AGS apoptosis and cell cycle assays were performed. To confirm the findings, oipA deletion mutant (ΔoipA) was generated and expression of VacA was detected using Western blotting. Result: Expression of AGS proteins involve in human disease was suppressed / down-regulated post-infection with oipA “off” strains, as well as oipA mutant, compared to oipA “on” strains. Furthermore, oipA “off” strains and oipA mutant resulted in a higher level of apoptosis and G0/G1 cell-cycle arrest in AGS cells than oipA “on” strains. Interestingly, deletion of oipA was found to increase VacA production by the bacterium. Discussion: The capability of oipA “off” strains to induce apoptosis and suppress proteins having roles in human disease may suggest that these H. pylori may be less virulent or may even be protective against carcinogenesis compared to its oipA “on” counterparts. This may potentially explain the higher incidence of gastric cancer among East Asian which oipA “on” strains predominates. Conclusions: Data from this study strengthened our understanding of the role of H. pylori OipA as a virulence factor in chronic inflammation, metastasis and carcinogenesis.

Dataset Information

Global gene expression of chemical carcinogen (N-methyl-N-nitrosourea), Helicobacter pylori infection, and high-salt diet-treated mouse gastric mucosa

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