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

ABSTRACT: Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE39490 | GEO | 2012/12/28

SECONDARY ACCESSION(S): PRJNA170979

REPOSITORIES: GEO

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

Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection. human Samples: Human gastric tumor cell line, N87 was grown in RPMI1640 supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-FOXD3 antibody. The immunoprecipitated-FOXD3 and -IgG DNA were used to probe the Agilent human ChIP-chip arrays. mouse Samples: Two-condition experiment, H pylori-infected vs. control gastric tissues. 2 dye-swap replicates.

2012-12-28 | E-GEOD-39490 | biostudies-arrayexpress

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

2012-12-28 | GSE39599 | GEO

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

Project description: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)

2012-12-28 | E-GEOD-39599 | biostudies-arrayexpress

Expression data from AGS cells with Helicobacter pylori infection

Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.

2024-04-18 | GSE264263 | GEO

Single-cell transcriptomic profiling uncovers cellular complexity and microenvironment in gastric tumorigenesis associated with Helicobacter pylori

Project description:Helicobacter pylori (H. pylori) infection is a key initiating factor in the Correa cascade of gastric carcinogenesis, but the comprehensive understanding of the pathogenic mechanisms underlying H. pylori-induced GC remains elusive. Here, we generated a single-cell atlas of gastric tumorigenesis comprising 18 specimens of gastritis, intestinal metaplasia and gastric cancer (GC) with or without H. pylori infection. We identified 48 distinct cell subpopulations including novel rare subtypes, and revealed the influence of H. pylori infection on cellular heterogeneity across neoplastic lesions.

2023-12-11 | GSE249874 | GEO

Remodeling of the gastric environment in Helicobacter pylori-induced atrophic gastritis

Project description:Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry (LC-MS/MS). We detected striking differences in protein content of corpus and antrum tissues. 492 proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared to infected corpus tissues with non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. Corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.

2023-12-04 | PXD046333 | Pride

mRNA microarray data from patients with non-active gastritis, chronic active gastritis and precursor lesions of gastric cancer

Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).

2020-09-01 | E-MTAB-8889 | biostudies-arrayexpress

miRNA sequencing data from patients with non-active gastritis, chronic active gastritis and precursor lesions of gastric cancer.

2020-09-01 | E-MTAB-8890 | biostudies-arrayexpress

small RNA sequencing data from patients with non-active gastritis, chronic active gastritis and precursor lesions of gastric cancer

2020-09-01 | E-MTAB-8896 | biostudies-arrayexpress

Expression data from Helicobacter pylori-infected mouse gastric epithelial progenitor and non-progenitor cells.

Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array

2008-02-22 | GSE10262 | GEO

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