2023 Fiscal Year Final Research Report
Development and functional analysis of a novel liver cancer model induced by metabolic stress
| Project/Area Number |
21K07135
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 50010:Tumor biology-related
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| Research Institution | Kindai University |
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Principal Investigator |
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 肝がん / メタボリック症候群 |
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| Outline of Final Research Achievements |
In recent years, there's been a global increase in liver cancers linked to non-alcoholic steatohepatitis (NASH), more associated with lifestyle diseases than with viral infections or autoimmune hepatitis. Many details, like the molecular mechanisms of liver cancer associated with metabolic syndrome and specific therapeutic targets, remain unclear. We analyzed the effects of liver-specific Bat3 deficiency in mice on liver cancer development and progression induced by a high-fat diet. Bat3 deficiency accelerated liver cancer, suggesting it involved activation of the MYC and EGF pathways, as shown by genetic analysis and mass spectrometry. Analysis of a human liver cancer database also revealed cases with BAT3 mutations.
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| Free Research Field |
癌、細胞死、エピジェネティクス
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| Academic Significance and Societal Importance of the Research Achievements |
近年、ウイルス性感染や自己免疫性肝炎よりも、生活習慣病に起因する非アルコール性脂肪肝炎に起因する肝癌の割合が世界的に増加傾向にある。しかしながらメタボリック症候群に伴う肝がん発症の分子機序の詳細、サブタイプ特異的な治療標的等、不明な点が多い。本研究の成果はNASHに伴う肝癌発症・進展にBAT3が重要な役割を果たすことが示唆され、今後の治療標的開発につながることが強く予想される。
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