PTEN at the crossroad of metabolic diseases and cancer in the liver

The tumor suppressor PTEN is a phosphoinositide phosphatase regulating the PI3K/Akt signaling pathways and mutated or deleted in a variety of human cancers. Recent evidence indicates that dysregulated PTEN expression and activity in the liver critically affect hepatic insulin sensitivity and trigger...

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Main Authors: Manlio Vinciguerra, Michelangelo Foti
Format: Article
Language:English
Published: Elsevier 2008-07-01
Series:Annals of Hepatology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1665268119318484
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spelling doaj-a66afe00ca8b4f269bc867b6a4d10c5b2021-06-09T05:56:06ZengElsevierAnnals of Hepatology1665-26812008-07-0173192199PTEN at the crossroad of metabolic diseases and cancer in the liverManlio Vinciguerra0Michelangelo Foti1Dept. Cellular Physiology and Metabolism, Geneva Medical Faculty, Geneva, Switzerland; EMBL Mouse Biology Unit, Monterotondo, Rome, Italy; Address for correspondence: Michelangelo Foti Department of Cellular Physiology and Metabolism CMU 1, rue Michel-Servet 1211 Geneva, Switzerland Tel.: +41/22/3795204 Fax: +41/22/3795260 E-mail:Dept. Cellular Physiology and Metabolism, Geneva Medical Faculty, Geneva, SwitzerlandThe tumor suppressor PTEN is a phosphoinositide phosphatase regulating the PI3K/Akt signaling pathways and mutated or deleted in a variety of human cancers. Recent evidence indicates that dysregulated PTEN expression and activity in the liver critically affect hepatic insulin sensitivity and trigger the development of non-alcoholic fatty liver diseases. As well, PTEN expression/activity is also affected with HBV and HCV infection, or following alcohol-related injury. Finally, PTEN mutations/deletions or low PTEN expression are associated with diverse liver malignancies thus suggesting a critical role for PTEN in hepatic cancers. This review will focus on our current knowledge of the regulation of PTEN expression/activity and the role of this phosphatase in liver diseases.http://www.sciencedirect.com/science/article/pii/S1665268119318484PTENinsulin resistancemetabolic syndromeobesitynon-alcoholic fatty liver diseasessteatosis
collection DOAJ
language English
format Article
sources DOAJ
author Manlio Vinciguerra
Michelangelo Foti
spellingShingle Manlio Vinciguerra
Michelangelo Foti
PTEN at the crossroad of metabolic diseases and cancer in the liver
Annals of Hepatology
PTEN
insulin resistance
metabolic syndrome
obesity
non-alcoholic fatty liver diseases
steatosis
author_facet Manlio Vinciguerra
Michelangelo Foti
author_sort Manlio Vinciguerra
title PTEN at the crossroad of metabolic diseases and cancer in the liver
title_short PTEN at the crossroad of metabolic diseases and cancer in the liver
title_full PTEN at the crossroad of metabolic diseases and cancer in the liver
title_fullStr PTEN at the crossroad of metabolic diseases and cancer in the liver
title_full_unstemmed PTEN at the crossroad of metabolic diseases and cancer in the liver
title_sort pten at the crossroad of metabolic diseases and cancer in the liver
publisher Elsevier
series Annals of Hepatology
issn 1665-2681
publishDate 2008-07-01
description The tumor suppressor PTEN is a phosphoinositide phosphatase regulating the PI3K/Akt signaling pathways and mutated or deleted in a variety of human cancers. Recent evidence indicates that dysregulated PTEN expression and activity in the liver critically affect hepatic insulin sensitivity and trigger the development of non-alcoholic fatty liver diseases. As well, PTEN expression/activity is also affected with HBV and HCV infection, or following alcohol-related injury. Finally, PTEN mutations/deletions or low PTEN expression are associated with diverse liver malignancies thus suggesting a critical role for PTEN in hepatic cancers. This review will focus on our current knowledge of the regulation of PTEN expression/activity and the role of this phosphatase in liver diseases.
topic PTEN
insulin resistance
metabolic syndrome
obesity
non-alcoholic fatty liver diseases
steatosis
url http://www.sciencedirect.com/science/article/pii/S1665268119318484
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