Abstract
Epigenetics, an inheritable phenomenon, which influences the expression of gene without altering the DNA sequence, offers a new perspective on the pathogenesis of hepatocellular carcinoma (HCC). Nonalcoholic steatohepatitis (NASH) is projected to account for a significant share of HCC incidence due to the growing prevalence of various metabolic disorders. One of the major molecular mechanisms involved in epigenetic regulation, post-translational histone modification seems to coordinate various aspects of NASH which will further progress to HCC. Mounting evidence suggests that the orchestrated events of cellular and nuclear changes during apoptosis can be regulated by histone modifications. This review focuses on the current advances in the study of acetylation-/methylation-mediated histone modification in apoptosis and the implication of these epigenetic regulations in HCC. The reversibility of epigenetic alterations and the agents that can target these alterations offers novel therapeutic approaches and strategies for drug development. Further molecular mechanistic studies are required to enhance information governing these epigenetic modulators, which will facilitate the design of more effective diagnosis and treatment options.
Highlights
Epigenetic phenomena are heritable adaptive reversible changes in gene expression, or the phenotype modulated by environmental stimuli, which are not induced by changes in the DNA sequence [1]
Studies in recent years have shown that epigenetic changes of the chromatin state are fundamental parameters of the nuclear rearrangements experienced by apoptotic cells that can be further responsible for various disease states including cancer [7,8,9]
This review focuses on the acetylation-/methylation-mediated post-translational histone modifications that have been shown to be regulated during apoptosis and its implications in nonalcoholic fatty liver disease (NAFLD) to Nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) pathogenesis
Summary
Epigenetic phenomena are heritable adaptive reversible changes in gene expression, or the phenotype modulated by environmental stimuli, which are not induced by changes in the DNA sequence [1]. The development of HCC is a complex process of dysregulated cellular and molecular events driven by genetic and epigenetic abnormalities [14,15,16]. The lifestyle aspects such as physical inactivity, over nutrition, metabolic disorders like insulin resistance, and weight gain are reported to influence the development and progression of NASH and HCC via epigenetic mechanisms [17,18]. This review focuses on the acetylation-/methylation-mediated post-translational histone modifications that have been shown to be regulated during apoptosis and its implications in NAFLD to NASH and HCC pathogenesis
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