Epigenetic dysregulation in autophagy signaling as a driver of viral manifested oral carcinogenesis

Abstract

BackgroundConcurrent viral infections insist on dysregulated epigenetics of tumor suppressor genes (TSGs), cell cycle regulators, apoptosis, and autophagy-associated genes to manifest oral carcinogenesis. Autophagy has been projected as a strategic defense signaling cascade against viral entry and subsequent oral carcinogenesis. Compromised autophagy signaling during viral infection fuels oral cancer initiation and progression. Scope of reviewThe aberrant expression of autophagy genes and their encoded proteins is catalyzed by the dysregulated epigenome, legitimate epigenomic mutations, and post-transcriptional modifications such as hypermethylation, deacetylation of histone and non-histone targets, and hyperacetylation of histones that drive malignant transformation during oral carcinogenesis. Recent investigations have predicted epi-drugs (intriguingly methylation and deacetylation inhibitors and activators) as next-generation oral cancer therapeutic agents with a special notation for autophagy regulation. Major conclusionsThis review focuses on the epigenetic mediated post-transcriptional modulation of autophagy genes during viral manifested oral carcinogenesis with a distinctive perception of autophagy-modulating epi-drugs in oral cancer therapeutics.