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Lozano-Rosas et al. Hepatoma Res 2018;4:19                       Hepatoma Research
               DOI: 10.20517/2394-5079.2018.48




               Review                                                                        Open Access


               Mitoepigenetics and hepatocellular carcinoma


               María Guadalupe Lozano-Rosas, Enrique Chávez, Alejandro Rusbel Aparicio-Cadena,
               Gabriela Velasco-Loyden, Victoria Chagoya de Sánchez
               Department of Cellular Biology and Development, Institute of Cellular Physiology, National Autonomous University of Mexico,
               Mexico City 04510, Mexico.
               Correspondence to: Dr. Victoria Chagoya de Sánchez, Department of Cellular Biology and Development, Institute of Cellular
               Physiology, National Autonomous University of Mexico, Mexico City 04510, Mexico. E-mail: vchagoya@correo.ifc.unam.mx

               How to cite this article: Lozano-Rosas MG, Chávez E, Aparicio-Cadena AR, Velasco-Loyden G, Chagoya de Sánchez V.
               Mitoepigenetics and hepatocellular carcinoma. Hepatoma Res 2018;4:19. http://dx.doi.org/10.20517/2394-5079.2018.48

               Received: 30 Apr 2018    First Decision: 21 May 2018    Revised: 7 Jun 2018    Accepted: 10 Jun 2018    Published: 19 Jun 2018
               Science Editor: Guang-Wen Cao    Copy Editor: Jun-Yao Li    Production Editor: Cai-Hong Wang



               Abstract
               Mitochondria are the center of energy production in eukaryotic cells and are crucial for several cellular processes.
               Dysfunctional mitochondria have been associated with cancer progression. Mitochondria contain their own circular
               DNA (mtDNA), which codes for 13 proteins, 2rRNA, 22tRNA and non-coding RNAs. Recent evidence showed the
               presence of 5-methylcytosine and 5-hydroximethylcytosine in mtDNA suggesting that the level of gene expression
               could be modulated like a nuclear DNA by direct epigenetic modifications. Mitoepigenetics is a bidirectional
               phenomenon in the epigenetic regulation of mitochondrial genes encoded in both the nucleus and the mitochondrion.
               This process is affected by SAM-mediated methylation and hydroxymethylation of mtDNA and by nuclear chromatin
                                                                +
               modulators from mitochondria, such as Acetyl-CoA and NAD . There is some information about physiological and
               pathological methylated profiles, but information is scarce for hepatocellular carcinoma (HCC). The aim of this review
               is to summarize the mitoepigenetic knowledge in HCC already reported so far, through a keywords search in Medline.
               In addition, the deregulation of energy intermediaries needed for the mitoepigenetic regulation is described. As this is a
               new area of study, a rigorous analysis and careful interpretation and integration of results are needed.

               Keywords: Hepatocellular carcinoma, mitochondrial genome, mitochondrial epigenome, microRNAs




               INTRODUCTION
               Hepatocellular carcinoma (HCC) is a highly malignant cancer, with high recurrence rate and a poor
               prognosis. HCC is a complex pathology associated with chronic liver disease, 80% to 90% are originated
               from cirrhosis of diverse etiology, most frequently infections with hepatitis B virus, hepatitis C virus, the
               mycotoxin, aflatoxin B1, and the metabolic syndrome .
                                                            [1,2]
                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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