Epigenetics in oral cancer-neoteric biomarker

Abstract

A cancer develops when a cell acquires specific growth advantages through the stepwise accumulation of heritable changes in gene function. Cancer genes may be changed by several mechanisms, which potentially alter the protein encoding nucleotide template, change the copy number of genes or leads to increased gene transcription. Epigenetic alterations are increasingly being recognized for their roles in carcinogenesis. Deregulation of gene expression is a hallmark of cancer. Although genetic lesions have been the focus of cancer research for many years, it has become increasingly recognized that aberrant epigenetic modifications also play major roles in the tumorigenic process. These modifications imposed on chromatin, do not change the nucleotide sequence of DNA, and are manifested by specific patterns of gene expression. The field of cancer epigenetics is evolving rapidly on several fronts. Advances in our understanding of chromatin structure, histone modification, and transcriptional activity and DNA methylation have resulted in an increasingly integrated view of epigenetics. Whilst genetic alterations in oral cancer have long been documented, the appreciation of epigenetic changes is more recent. Epigenetic changes alter expression of tumour suppressor genes without changes in DNA sequence. Epigenetic mechanisms such as DNA methylation, histone methylation and deacetylation have been shown to silence key genes involved in cell proliferation, differentiation and genome integrity and clearly have a central role in oral cancer. Epigenetics is another major player in multistep carcinogenesis of oral cancers. In this article we discuss current literature in the field of the epigenetics of oral cancer, placing a great deal of emphasis on DNA methylation, histone modification and post-transcriptional gene down-regulation by microRNAs.