Epigenetics Research: Open Access

Epigenetics Research: Open Access
Open Access

DNA methylation

Cancer linked DNA hypo-methylation and hyper-methylation are present throughout the human genome. The hyper-methylation facilitates cancer progress by repressing the tumor suppressor gene. Hypo-methylation contribution towards cancer has not yet been clear. Recent studies of tissue specific methylation have suggested that DNA hypo-methylation aid tumor formation by many pathways. Loss of DNA methylation associated with cancer may alter transcription. In addition, DNA hypo-methylation might affect promoter usage production of intra-genic non-coding RNA transcripts, co-transcriptional splicing and initiation and elongation of transcription. Studies of hemi methylation of DNA in cancerous cells as well as normal tissues suggest that active de-methylation can explain cancer associated DNA hypo-methylation. New studies that genomic 5-hydroxymethylcytosine is intermediate in DNA de-methylation exhibits cancer associated losses. It suggests that both decreased hydroxyl-methylation and methylation of DNA play important role in carcinogenesis.