Epigenetic mechanisms as a new approach in cancer treatment: An updated review

Abstract

Epigenetic, along with genetic mechanisms, is essential for natural evolution and maintenance of specific patterns of gene expression in mammalians. Global epigenetic variation is inherited somatically and unlike genetic variation, it is dynamic and reversible. They are somatically associated with known genetic variations. Recent studies indicate the broad role of epigenetic mechanisms in the initiation and development of cancers, that they are including DNA methylation, histone modifications, nucleosomes changes, non-coding RNAs. The reversible nature of epigenetic changes has led to the emergence of novel epigenetic therapeutic approaches, so that several types of these medications have been approved by the FDA so far. In this review, we discuss the concept of epigenetic changes in diseases, especially cancers, the role of these changes in the onset and progression of cancers and the potential of using this knowledge in designing novel therapeutic strategies.

Keywords: Cancer; Epigenetic; Mechanisms; Methylation; Treatment.

Figure 1

The role of epigenetics changes in diseases and related therapeutic agents: Histone acetylation is associated with the opening of the chromatin mass and the onset of transcription, while deacetylation do the opposite, but the methylation of histones, like DNA methylation condenses chromatin and accompanies transcriptional inhibition. Reversion of each related epigenetics condition with appropriate inhibitor can reverse disease symptoms.

Figure 2

Collaboration of PRC1 and PRC2 in suppressing transcription: The PRC2 with its main subunit (EZH2) triggers H3K27 trimetylation. PRC1 via chromobox (CBX) interacts with H3K27me3 and catalyzes the ubiquitination of H2AK119. So the expression of genes such as the tumor suppresor genes (TSGs) is inhibited and one of the hits for tumor initiation is performed.