Editorial DNA Methylation Induced Epigenetic Silencing: A Potential Biomarker and Therapeutic Target for Head and Neck Squamous Cell Carcinoma

How to cite the article: Patil S, Rao R, Raj T. DNA methylation induced epigenetic silencing: A potential biomarker and therapeutic target for head and neck squamous cell carcinoma. J Int Oral Health 2015;(4):i-ii DNA methylation is a physiologic process in which the dinucleotides outside the CpG islands are methylated while the CpG islands with promoter regions remain non-methylated. This specific pattern of DNA methylation is called “methylotype” or the basic genomic methylation pattern. The process is catalyzed by a group of enzymes called DNA methyltransferases (DNMTs: DNMT1, DNMT3A and DNMT3B). DNMTs 3A and 3B are responsible for de novo methylation and DNMT1 for the maintenance of the methylation pattern of the template strand. Variation from “methylotype ” represents an epigenetic aberration, causing an altered gene expression without changing the actual DNA sequence.1 A shift in the methylation pattern may follow one of the following paths: Increased methylation of the promoter regions of CpG islands causing repression of genes involved in DNA repair, apoptosis, tumor suppression and cell cycle regulation (or) loss of methylation of oncogenes causing its overexpresion. A shift in the “methylotype ” may lead to genetic instability and initiate carcinogenesis. Kozaki et al. observed that the epigenetic silencing of tumor suppressive miRNA including miR-34b, miR-137, miR-193a, and miR-203 was a common event in oral cancer.2 Recent studies have found more than 30 altered miRNA genes due to aberrant DNA methylation patterns.2-5 Baba et al. demonstrated that the CHFR gene, responsible for providing checkpoint at the G2-M transition, is significantl