Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [MMASS]

ABSTRACT: Promoter hypermethylation occurs in human gastric cancers, but whether the deregulated genes contribute to the multi-step Helicobacter pylori (H pylori)-induced gastric carcinogenesis remains unclear. We used Microarray-based Methylation Assessment of Single Samples (MMASS) to identify differential methylated genes in 10 human gastric cancer tissues. Two-condition experiment, gastric cancers from patients (n = 5 per group) who survived 5 years or more (long-term survivors group) and who died of disease prior to 5 years (short-term survivors group)

ORGANISM(S): Homo sapiens

SUBMITTER: Alfred Cheng

PROVIDER: E-GEOD-39599 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Helicobacter pylori causes epigenetic dysregulation of FOXD3 to promote gastric carcinogenesis.

Cheng Alfred S L AS Li May S MS Kang Wei W Cheng Victoria Y VY Chou Jian-Liang JL Lau Suki S SS Go Minnie Y MY Lee Ching C CC Ling Thomas K TK Ng Enders K EK Yu Jun J Huang Tim H TH To Ka F KF Chan Michael W MW Sung Joseph J Y JJ Chan Francis K L FK

Gastroenterology 20121008 1

<h4>Background & aims</h4>Deregulation of forkhead box (Fox) proteins, an evolutionarily conserved family of transcriptional regulators, leads to tumorigenesis. Little is known about their regulation or functions in the pathogenesis of gastric cancer. Promoter hypermethylation occurs during Helicobacter pylori-induced gastritis. We investigated whether the deregulated genes contribute to gastric tumorigenesis.<h4>Methods</h4>We used integrative genome-wide scans to identify concomitant hypermeth ...[more]

PMID: 23058321

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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

Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [MMASS]

Publications

Helicobacter pylori causes epigenetic dysregulation of FOXD3 to promote gastric carcinogenesis.

Similar Datasets

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