期刊
CURRENT MOLECULAR MEDICINE
卷 7, 期 1, 页码 85-102出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/156652407779940413
关键词
DNA methylation; cancer; chromatin; promoter methylation; 5-aza-2 '-deoxycytidine; hypermethylation; hypomethylation; repetitive elements; virus; preneoplasia
资金
- NCI NIH HHS [U01CA84971, P50 CA070907, P50CA75907] Funding Source: Medline
The spatial arrangement and three-dimensional structure of DNA in the nucleus is controlled through the interdigitation of DNA binding proteins such as histones and their modifiers, the Polycomb-Trithorax proteins, and the DNA methyltransferase enzymes. DNA methylation forms the foundation of chromatin and is crucial to epigenetic gene regulation in mammals. Disease pathogenesis mediated through infectious agents, inflammation, aging, or genetic damage often involves changes in gene expression. In particular, cellular transformation coincides with multiple changes in chromatin architecture, many of which appear to affect genome integrity and gene expression. Infectious agents, such as viruses directly affect genome structure and induce methylation of particular sequences to suppress host immune responses. Hyperproliferative tissues such as those in the gastrointestinal tract and colon have been shown to gradually acquire aberrant promoter hypermethylation. Here we review recent findings on altered DNA methylation in human disease, with particular focus on cancer and the increasingly large number of genes subject to tumor-specific promoter hypermethylation and the possible role of aberrant methylation in tumor development.
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