Abstract |
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.
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Authors | Manlio Vinciguerra, Michelangelo Foti |
Journal | Annals of hepatology
(Ann Hepatol)
2008 Jul-Sep
Vol. 7
Issue 3
Pg. 192-9
ISSN: 1665-2681 [Print] Mexico |
PMID | 18772845
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Enzyme Inhibitors
- Insulin
- Phosphatidylinositol 3-Kinases
- Proto-Oncogene Proteins c-akt
- PTEN Phosphohydrolase
- PTEN protein, human
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Topics |
- Enzyme Inhibitors
(pharmacology)
- Fatty Liver
(enzymology)
- Gene Expression Regulation, Enzymologic
- Gene Expression Regulation, Neoplastic
- Hepatitis B
(enzymology)
- Hepatitis C
(enzymology)
- Humans
- Insulin
(metabolism)
- Insulin Resistance
- Liver
(drug effects, enzymology)
- Liver Diseases
(drug therapy, enzymology, genetics)
- Liver Diseases, Alcoholic
(enzymology)
- Liver Neoplasms
(drug therapy, enzymology, genetics)
- Mutation
- PTEN Phosphohydrolase
(antagonists & inhibitors, genetics, metabolism)
- Phosphatidylinositol 3-Kinases
(metabolism)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Signal Transduction
(drug effects, genetics)
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