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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Alfred Cheng 

PROVIDER: E-GEOD-39490 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress