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      The Role of Histone Acetylation-/Methylation-Mediated Apoptotic Gene Regulation in Hepatocellular Carcinoma

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          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.

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          The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases.

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            Defining the role of hypoxia-inducible factor 1 in cancer biology and therapeutics.

            Adaptation of cancer cells to their microenvironment is an important driving force in the clonal selection that leads to invasive and metastatic disease. O2 concentrations are markedly reduced in many human cancers compared with normal tissue, and a major mechanism mediating adaptive responses to reduced O2 availability (hypoxia) is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). This review summarizes the current state of knowledge regarding the molecular mechanisms by which HIF-1 contributes to cancer progression, focusing on (1) clinical data associating increased HIF-1 levels with patient mortality; (2) preclinical data linking HIF-1 activity with tumor growth; (3) molecular data linking specific HIF-1 target gene products to critical aspects of cancer biology and (4) pharmacological data showing anticancer effects of HIF-1 inhibitors in mouse models of human cancer.
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              Cancer epigenetics: from mechanism to therapy.

              The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15 years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it is time to embrace the central role of epigenetics in cancer. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                24 November 2020
                December 2020
                : 21
                : 23
                : 8894
                Affiliations
                [1 ]Department of Surgery, Marshall University School of Medicine, Huntington, WV 25701, USA; rajan@ 123456marshall.edu (P.K.R.); udohu@ 123456marshall.edu (U.-A.U.); sanabriaju@ 123456marshall.edu (J.D.S.); smith2152@ 123456live.marshall.edu (G.S.); schade4@ 123456live.marshall.edu (M.S.S.); sanabriaja@ 123456marshall.edu (J.S.); sodhi@ 123456marshall.edu (K.S.)
                [2 ]Marshall Institute for Interdisciplinary Research (MIIR), Marshall University School of Medicine, Huntington, WV 25701, USA; banerjeem@ 123456marshall.edu (M.B.); pierres@ 123456marshall.edu (S.P.); xiez@ 123456marshall.edu (Z.X.); shapiroj@ 123456marshall.edu (J.I.S.)
                Author notes
                [* ]Correspondence: sanabriaj@ 123456marshall.edu ; Tel.: +1-(216)-647-8399
                [†]

                In memory of a scientist and mentor.

                Author information
                https://orcid.org/0000-0002-1179-2985
                Article
                ijms-21-08894
                10.3390/ijms21238894
                7727670
                33255318
                98854e28-b82b-4ea8-9191-7d7ec821322f
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 13 October 2020
                : 16 November 2020
                Categories
                Review

                Molecular biology
                histone modification,histone acetylation,histone methylation,nafld,nash,hcc
                Molecular biology
                histone modification, histone acetylation, histone methylation, nafld, nash, hcc

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