DNA Methylation in Colorectal Cancer: A brief Review

Abstract

In human tumors, epigenetic modifications, particularly DNA methylation in specific gene promoters, are recognized as common molecular alterations. In concert with other epigenetic mechanisms, DNA methylation acts to regulate gene expression and facilitate chromatin organization within cells. Substantial research has been done to determine the cause and role of aberrant DNA methylation (“epigenomic instability”) in colon cancer. During carcinogenesis, epigenetic switching and 5'-methylcytosine reprogramming result in the hypermethylation of CpG islands, reducing epigenetic plasticity of critical developmental and tumor suppressor genes, rendering them unresponsive to normal stimuli. For early detection of cancer, quantitative approaches to identify DNA methylation differences between normal and cancer tissues could lead to the identification of a panel of highly

specific methylated markers. Since it has been well established that genetic and epigenetic alterations influence the development of colorectal cancer (CRC), so to improve the current diagnosis, screening, prognosis and treatment prediction for the disease huge potential lies in the use of DNA methylation as a biomarker. Also, for therapy prediction, more studies should focus on finding markers for chemotherapeutic drugs as majority of the patients would be benefited.