ABSTRACT
DNA methylation comprises an integral part of epigenetics and its gene silencing effects have been implicated in numerous biological processes such as aging, development, memory formation, and oncogenesis. DNA methylation is carried out by the DNA methyltransferase (DNMT) family of enzymes, which transfer methyl groups from S-adenosylmethionine to the 5-position of cytosine in CpG dinucleotides [1]. Hypermethylation during oncogenesis usually occurs at CpGs located in CpG islands, which are C-G rich regions of 300-3000 bp in or near 40% of promoters in mammalian genes [1]. About 70% of the promoters of human genes contain CpG islands within close proximity. The product of DNA methylation, 5-methylcytosine, is highly susceptible to mutation due to spontaneous deamination, which results in a cytosine to thymine mutation. CpG conversion to TpG over most of the genome has led to highly conserved regions of DNA in or near promoter regions that contain an unusually high percentage of CpGs. These regions are normally unmethylated and the lack of methylation has prevented accumulation of C!T mutations and has promoted the formation of CpG islands [2]. DNA methylation allows an additional tier of hereditable genetic information to be stored upon the genetic code of DNA without changes in the DNA sequence itself. The accepted paradigm of DNA methylation is that hypermethylation usually leads to silencing of gene activity, while the expression of a few genes may be activated by DNA methylation.
