Ampuero J, Romero-Gomez M. Prevention of hepatocellular carcinoma by correction of metabolic abnormalities: Role of statins and metformin. World J Hepatol 2015; 7(8): 1105-1111 [PMID: 26052399 DOI: 10.4254/wjh.v7.i8.1105]
Corresponding Author of This Article
Javier Ampuero, MD, PhD, Unit for the Clinical Management of Digestive Diseases, Valme University Hospital, Avenida de Bellavista s/n, 41014 Sevilla, Spain. javi.ampuero@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
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/
World J Hepatol. May 18, 2015; 7(8): 1105-1111 Published online May 18, 2015. doi: 10.4254/wjh.v7.i8.1105
Prevention of hepatocellular carcinoma by correction of metabolic abnormalities: Role of statins and metformin
Javier Ampuero, Manuel Romero-Gomez
Javier Ampuero, Manuel Romero-Gomez, Unit for the Clinical Management of Digestive Diseases, Valme University Hospital, 41014 Sevilla, Spain
Author contributions: Ampuero J and Romero-Gomez M contributed to this paper.
Conflict-of-interest: No conflict of interest.
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: Javier Ampuero, MD, PhD, Unit for the Clinical Management of Digestive Diseases, Valme University Hospital, Avenida de Bellavista s/n, 41014 Sevilla, Spain. javi.ampuero@gmail.com
Telephone: +34-955-015761 Fax: +34-955-015899
Received: August 17, 2014 Peer-review started: August 18, 2014 First decision: September 16, 2014 Revised: January 18, 2015 Accepted: January 30, 2015 Article in press: February 2, 2015 Published online: May 18, 2015 Processing time: 275 Days and 10.4 Hours
Core Tip
Core tip: Hepatocellular carcinoma is the result of a complex process which impairs several pathways, such as RAS/RAF/mitogen-activated protein kinase kinase/extracellular-signal-regulated kinase, phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mammalian target of rapamycin and Wnt/β-catenin signaling. Patients showing metabolic syndrome seem to have higher incidence and mortality rates from hepatocellular carcinoma than healthy subjects, especially those with type 2 diabetes mellitus and obesity. Thus, metformin and statins, both to treat features of metabolic syndrome, have been proposed to decrease the risk of hepatocellular carcinoma. Metformin (by decreasing hyperglycemia state through 5′-adenosine monophosphate-activated protein kinase pathway activation) and statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) show anti-tumoral properties modifying several steps of the crucial signaling cascades.
