Awad A, Gassama-Diagne A. PI3K/SHIP2/PTEN pathway in cell polarity and hepatitis C virus pathogenesis. World J Hepatol 2017; 9(1): 18-29 [PMID: 28105255 DOI: 10.4254/wjh.v9.i1.18]
Corresponding Author of This Article
Ama Gassama-Diagne, MD, Inserm Unité 1193, Hôpital Paul Brousse, 12 Avenue Paul Vaillant Couturier, 94800 Villejuif, France. ama.gassama@inserm.fr
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Review
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. Jan 8, 2017; 9(1): 18-29 Published online Jan 8, 2017. doi: 10.4254/wjh.v9.i1.18
PI3K/SHIP2/PTEN pathway in cell polarity and hepatitis C virus pathogenesis
Aline Awad, Ama Gassama-Diagne
Aline Awad, Ama Gassama-Diagne, Inserm Unité 1193, Hôpital Paul Brousse, 94800 Villejuif, France
Aline Awad, Ama Gassama-Diagne, Univ Paris-Sud, UMR-S 1193, Univsité Paris-Saclay, 94800 Villejuif, France
Author contributions: Awad A and Gassama-Diagne A discussed the ideas; Awad A wrote the manuscript; Gassama-Diagne A edited the manuscript.
Supported byAgence Nationale de Recherche sur le Sida et les hépatites (ANRS, France), Ligue contre le cancer, France.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
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: Ama Gassama-Diagne, MD, Inserm Unité 1193, Hôpital Paul Brousse, 12 Avenue Paul Vaillant Couturier, 94800 Villejuif, France. ama.gassama@inserm.fr
Telephone: +33-14-5596070 Fax: +33-14-5596090
Received: June 28, 2016 Peer-review started: June 30, 2016 First decision: August 10, 2016 Revised: September 10, 2016 Accepted: November 1, 2016 Article in press: November 2, 2016 Published online: January 8, 2017 Processing time: 191 Days and 9.2 Hours
Core Tip
Core tip: Chronic hepatitis C virus (HCV) infection leads to liver cirrhosis and cancer. HCV infection modulates the lipid metabolism. Phosphoinositides are minor phospholipids that are also modified by HCV infection. phosphatidylinositol (PtdIns)(3,4,5)P3 is mainly formed by phosphoinositide 3-kinase (PI3K), and can be dephosphorylated by SH2-containing inositol polyphosphate 5-phosphatase (SHIP2) to generate PtdIns(3,4)P2. In this review, we will discuss the effects of SHIP2 and PI3K on the formation of cell polarity and how their expression and activation are modulated by HCV infection, leading to the disruption of cell polarity. This pathway is also discussed in the event of insulin resistance and nonalcoholic fatty liver disease related to HCV infection.
