Genome-wide analysis of DNA methylation profile provides clinical implication of Crohn’s Disease
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ABSTRACT: Inflammatory bowel disease (IBD) is known to be caused by a genetic predisposition involving multiple genes; however, there is growing evidence that abnormal interaction with environmental, particularly epigenetic, factors can have a significant contribution during the development of IBD. Although many studies, particularly genome-wide association studies (GWAS), have been performed to identify the genetic changes underlying the pathogenesis of Crohn’s disease (CD), the role of epigenetic changes in the development of complications arising from CD is poorly understood. Here, we employed an unbiased approach to define DNA methylation alteration in CD patients using the HumanMethylation450K BeadChip platform. Compared to normal controls, the majority of differential DNA methylation in CD patient samples was in the promoter, intergenic, and gene body regions. The DNA methylation profile in CD revealed 134 probes (23 hypermethylated and 111 hypomethylated probes) that were differentially methylated. We validated the methylation levels of 19 genes that showed hypermethylation in CD patients compared with normal control. Technical validation was performed using quantitative MSP analysis and we finally identified that the Fragile Histidine Triad (FHIT) genes were hypermethylated in a disease-specific manner. Gene network analysis of the hypermethylated candidates suggested putative molecular interactions relevant to IBD pathology. Overall, our DNA methylation profile identifies newly hypermethylated genes in CD, as well as the gene network associated with disease development, which can provide new therapeutic targets.
ORGANISM(S): Homo sapiens
PROVIDER: GSE105798 | GEO | 2017/12/25
SECONDARY ACCESSION(S): PRJNA415432
REPOSITORIES: GEO
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