Editorial: The Role of Epigenetic Modifications in Cancer Progression.

Abstract

Epigenetics describes multimodal molecular mechanisms that confer a certain phenotype on cell without a change in genotype (1). Chromatin remodelers (e.g. SWI/SNF complex) control opening and shutting a gateway for transcription factors to access genomic loci, and chemical modifications on chromatins (e.g. DNA methylation and histone modifications) regulate transcriptional activities, both resulting in a large-scale alteration of transcriptional landscape (2,3). Small noncoding RNAs also modulate a transcriptome by targeting a large number of sequence-matched mRNAs and sustain an epigenetic state by triggering and maintaining epigenetic gene silencing of chromatin modifier (4).In the post-genomic era, epigenetic regulations have been widely investigated to understand the molecular mechanisms underlying transcriptional addiction and phenotypic diversity in cancer cells. In this research topic, we have organized a collection of reviews and original research articles that shed light on the epigenetic regulations of cancer cell identity and fate. Chemical modifications in histone proteins, such as acetylation, methylation, phosphorylation, and ubiquitination, alter the structure of chromatin and renew the transcriptional landscape. Since the manner of histone modifications is often dysregulated in cancer, understanding the molecular mechanism by which the modifications contribute to cancer progression is important. Illiano et al.