title: [Tumor suppressor gene PTEN and non-alcoholic steatohepatitis (NASH)].
abstract: Although hepatic steatosis had been considered to be a benign condition that does not deteriorate to either liver cirrhosis or hepatocellular carcinoma (HCC). Non-alcoholic steatohepatitis (NASH) is notable disease that has similar pathological features to alcoholic liver injury and progresses to liver cirrhosis and HCC. But the molecular mechanism for the onset of NASH, and for the transformation from steatosis to carcinogenesis are still unclear. Hepatocyte-specific PTEN deficient mice, we generated, have similar histological features to the patients of human NASH. These hepatocytes showed enhanced lipid accumulation, inflammatory change, and hyperoxidation. Moreover, they developed into HCC. Thus, impairment of PI3K/PTEN signaling may possibly be involved in a part of NASH/HCC cases in human.
authors.affiliation: Department of Gastroenterology, Akita University School of Medicine.
authors.forename: Wataru
authors.initials: W
authors.lastname: Sato
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Horie
authors.forename: Sumio
authors.initials: S
authors.lastname: Watanabe
authors.forename: Akira
authors.initials: A
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D016207:Cytokines / Q000502:physiology; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D016147:Genes, Tumor Suppressor; D022781:Hepatocytes / Q000378:metabolism / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D050356:Lipid Metabolism; D008113:Liver Neoplasms / Q000235:genetics*; D051379:Mice; D018384:Oxidative Stress / Q000235:genetics; D051059:PTEN Phosphohydrolase; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D010744:Phosphoric Monoester Hydrolases / Q000172:deficiency / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000172:deficiency / Q000502:physiology*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D025521:Tumor Suppressor Proteins; D019869:Phosphatidylinositol 3-Kinases; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human