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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Jun 18, 2015; 7(11): 1530-1540
Published online Jun 18, 2015. doi: 10.4254/wjh.v7.i11.1530
MicroRNAs dysregulation in hepatocellular carcinoma: Insights in genomic medicine
Iván Lyra-González, Laura E Flores-Fong, Ignacio González-García, David Medina-Preciado, Juan Armendáriz-Borunda
Iván Lyra-González, Laura E Flores-Fong, Ignacio González-García, David Medina-Preciado, Juan Armendáriz-Borunda, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Instituto de Biología Molecular en Medicina y Terapia Génica, Guadalajara, Jalisco 44281, México
Ignacio González-García, O.P.D. Hospital Civil de Guadalajara “Fray Antonio Alcalde”, Guadalajara, Jalisco 44281, México
David Medina-Preciado, O.P.D. Hospital Civil de Guadalajara “Juan I. Menchaca”, Guadalajara, Jalisco 44281, México
Juan Armendáriz-Borunda, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Guadalajara, Jalisco 44281, México
Author contributions: All the authors equally contributed to this work.
Conflict-of-interest: Authors have no conflict of interests related to this manuscript. All authors have contributed equally in the realization of this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Juan Armendariz-Borunda, PhD, Head, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Sierra Mojada # 950, Guadalajara, Jalisco 44281, Mexico. armdbo@gmail.com
Telephone: +52-33-10585317 Fax: +52-33-10585318
Received: September 17, 2014
Peer-review started: September 20, 2014
First decision: November 27, 2014
Revised: December 22, 2014
Accepted: May 8, 2015
Article in press: May 11, 2015
Published online: June 18, 2015
Abstract

Hepatocellular carcinoma (HCC) is the leading primary liver cancer and its clinical outcome is still poor. MicroRNAs (miRNAs) have demonstrated an interesting potential to regulate gene expression at post-transcriptional level. Current findings suggest that miRNAs deregulation in cancer is caused by genetic and/or epigenetic, transcriptional and post-transcriptional modifications resulting in abnormal expression and hallmarks of malignant transformation: aberrant cell growth, cell death, differentiation, angiogenesis, invasion and metástasis. The important role of miRNAs in the development and progression of HCC has increased the efforts to understand and develop mechanisms of control overt this single-stranded RNAs. Several studies have analyzed tumoral response to the regulation and control of deregulated miRNAs with good results in vitro and in vivo, proving that targeting aberrant expression of miRNAs is a powerful anticancer therapeutic. Identification of up and/or down regulated miRNAs related to HCC has led to the discovery of new potential application for detection of their presence in the affected organism. MiRNAs represent a relevant new target for diagnosis, prognosis and treatment in a wide variety of pathologic entities, including HCC. This manuscript intends to summarize current knowledge regarding miRNAs and their role in HCC development.

Keywords: Hepatocellular carcinoma, MicroRNAs, Regulation, Therapeutic targets

Core tip: MicroRNAs are implicated in the control of gene expression which enable them a relevant new target for diagnosis, prognosis and treatment in a wide variety of pathologic entities, including hepatocellular carcinoma (HCC). This manuscript represents an attempt to summarize current knowledge regarding miRNAs and their role in HCC development.