CanMethdb: a database for genome-wide DNA methylation annotation in cancers

Abstract

Motivation DNA methylation within gene body and promoters in cancer cells is well documented. An increasing number of studies showed that cytosine-phosphate-guanine (CpG) sites falling within other regulatory elements could also regulate target gene activation, mainly by affecting transcription factors (TFs) binding in human cancers. This led to the urgent need for comprehensively and effectively collecting distinct cis-regulatory elements and TF-binding sites (TFBS) to annotate DNA methylation regulation. Results We developed a database (CanMethdb, http://meth.liclab.net/CanMethdb/) that focused on the upstream and downstream annotations for CpG–genes in cancers. This included upstream cis-regulatory elements, especially those involving distal regions to genes, and TFBS annotations for the CpGs and downstream functional annotations for the target genes, computed through integrating abundant DNA methylation and gene expression profiles in diverse cancers. Users could inquire CpG–target gene pairs for a cancer type through inputting a genomic region, a CpG, a gene name, or select hypo/hypermethylated CpG sets. The current version of CanMethdb documented a total of 38,986,060 CpG–target gene pairs (with 6,769,130 unique pairs), involving 385,217 CpGs and 18,044 target genes, abundant cis-regulatory elements, and TFs for 33 TCGA cancer types. CanMethdb might help biologists perform in-depth studies of target gene regulations based on DNA methylations in cancer. Availability The main program is available at https://github.com/chunquanlipathway/CanMethdb. Supplementary Information Supplementary data are available at Bioinformatics online.

Functional significance of DNA methylation: epigenetic insights into Sjögren’s syndrome

“…As a crucial regulator in the development and differentiation of immune cells, impaired DNA methylation profiles may substantially induce autoreactivity in the immune cells. This predisposes a person to immune irregularities and increases the possibility of progression in autoimmune anomalies (44)(45)(46). Epigenetic modification via DNA methylation recently gained consideration as a potential biomarker (47, 48).…”