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2016 Fiscal Year Final Research Report

Elucidating mechanisms specific to NASH-associated HCC development

Research Project

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Project/Area Number 15K12698
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Applied health science
Research InstitutionKanazawa University

Principal Investigator

Ota Tsuguhito  金沢大学, 脳・肝インターフェースメディシン研究センター, 准教授 (60397213)

Project Period (FY) 2015-04-01 – 2017-03-31
Keywords機能性脂質 / スフィンゴシンキナーゼ / 非アルコール性脂肪肝炎 / 肝がん / スフィンゴシン1リン酸
Outline of Final Research Achievements

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. It is characterized by a wide spectrum of hepatic changes, which may progress to non-alcoholic steatohepatitis (NASH) and cirrhosis. Ectopic fat or lipotoxicity in the liver can cause NASH-associated hepatocellular carcinoma (HCC). However, its underlying mechanism is unclear. In this study, we studied the role of a functional bioactive lipid ‘S1P’and its rate-limiting enzyme sphingosine kinase (SphK) in the development of NASH-associated HCC. We found that SphK activity and mRNA expression increased in the liver of both NASH mice and NASH patients compared those in normal liver. By contrast, knockdown of SphK led to suppress HCC development in hepatoma cell lines. Moreover, we found that diet or chemical-induced carcinogenesis in the liver were significantly decreased in SphK knockout mice compared to that in control mice. Thus, SphK might be a novel therapeutic target of NASH-associated HCCs.

Free Research Field

内分泌代謝学

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Published: 2018-03-22  

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