PI3K/SHIP2/PTEN pathway in cell polarity and hepatitis C virus pathogenesis

doi:10.4254/wjh.v9.i1.18

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World Journal of Hepatology

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1948-5182

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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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 by Agence 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.

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.