Journal
EPIGENETICS
Volume 13, Issue 4, Pages 386-397Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15592294.2018.1460034
Keywords
Epigenetic regulation; colorectal cancer; DNA methylation; gene expression; prediction model; HMGA1
Funding
- Matthias Lackas Foundation
- German Cancer Consortium (DKTK)
- Division of Preventive Oncology at the German Cancer Research Center (DKFZ)
- German Ministry of Education and Research (BMBF) within the e:Med consortium DeCaRe-Delineating Cardiac Regeneration
- Excellence cluster EXC 306 Inflammation at Interfaces of the German Science Foundation (DFG)
- Melanie Boerries the collaborative research center (CRC) [850]
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DNA methylation is recognized as one of several epigenetic regulators of gene expression and as potential driver of carcinogenesis through gene-silencing of tumor suppressors and activation of oncogenes. However, abnormal methylation, even of promoter regions, does not necessarily alter gene expression levels, especially if the gene is already silenced, leaving the exact mechanisms of methylation unanswered. Using a large cohort of matching DNA methylation and gene expression samples of colorectal cancer (CRC; n = 77) and normal adjacent mucosa tissues (n = 108), we investigated the regulatory role of methylation on gene expression. We show that on a subset of genes enriched in common cancer pathways, methylation is significantly associated with gene regulation through gene-specific mechanisms. We built two classification models to infer gene regulation in CRC from methylation differences of tumor and normal tissues, taking into account both gene-silencing and gene-activation effects through hyper - and hypo-methylation of CpGs. The classification models result in high prediction performances in both training and independent CRC testing cohorts (0.92
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