Publications
Detailed Information
Helicobacter pylori-infection-associated CpG island hypermethylation in the stomach and its possible association with polycomb repressive marks
Cited 25 time in
Web of Science
Cited 26 time in Scopus
- Authors
- Issue Date
- 2008-03-13
- Publisher
- Springer Verlag
- Citation
- Virchows Arch. 452(5):515-524
- Keywords
- Adult ; Aged ; Aged, 80 and over ; Alu Elements/genetics ; Carrier Proteins/genetics ; CpG Islands/*genetics ; DNA/genetics/metabolism ; DNA, Neoplasm/genetics/metabolism ; Gastritis/*genetics/microbiology ; Helicobacter Infections/*genetics ; Histones/genetics ; Humans ; Long Interspersed Nucleotide Elements/genetics ; Middle Aged ; Nuclear Proteins/genetics ; Repressor Proteins/*genetics ; Stomach Neoplasms/*genetics/microbiology ; DNA Methylation ; Helicobacter pylori
- Abstract
- Helicobacter pylori infection can induce CpG island (CGI) hypermethylation in gastric mucosa. Recently, genes occupied by Polycomb proteins in embryonic stem cells were shown to be vulnerable to aberrant DNA hypermethylation in cancers. To explore the relationship between H. pylori infection and DNA methylation changes in neoplastic and non-neoplastic stomach, we analyzed 25 CGIs and repetitive DNA elements from 82 chronic gastritis and 69 gastric carcinomas. Twenty-three CGIs showed significantly higher methylation levels in H. pylori-negative gastric carcinoma (n = 28) than in H. pylori-negative chronic gastritis (n = 39; P < 0.05), indicating cancer-associated methylation. Eight CGIs exhibited significantly higher methylation levels in H. pylori-positive chronic gastritis (n = 43) than in H. pylori-negative chronic gastritis (n = 39; P < 0.05). Six CGIs showed both cancer-associated and H. pylori-associated hypermethylation. Six (75%) of the eight H. pylori-associated hypermethylated genes contained at least one of three repressive marks (Suzl2 occupancy, Eed occupancy, histone H3 K27 trimethylation), whereas 31% of the remaining cancer-associated hypermethylated genes had at least one mark. The findings suggest that H. pylori infection strongly induces CGI hypermethylation in gastric epithelial cells and that susceptibility to H. pylori-induced DNA hypermethylation may be determined by Polycomb repressive marks in stem or progenitor cells.
- ISSN
- 0945-6317 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18335237
http://www.springerlink.com/content/4vm1324j4r512246/fulltext.pdf
https://hdl.handle.net/10371/67959
- Files in This Item:
- There are no files associated with this item.
- Appears in Collections:
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.