| Project/Area Number |
20K07406
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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 49020:Human pathology-related
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| Research Institution | Gifu University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2022: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2021: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ARID1A / T-cadherin / adiponectin / 大腸癌 / 乳癌 / Harakiri / NF-kB / ARID1a / メタボリック症候群 / クロマチン再構成機能異常 / クロマチン再構成因子複合体 |
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| Outline of Research at the Start |
メタボリック症候群、肥満状態における癌発生、進行とクロマチン再構成機能異常との関係は、個別に研究・報告されてきたため、両者の知見は橋渡しされてこなかった。
本研究は病理学的観点から、メタボリック症候群でARID1A発現不良が、乳癌、大腸癌進行にかかわるのかを明らかにすることを目的とする。
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| Outline of Final Research Achievements |
ARID1A is a DNA binding element of chromatin remodeling complex, human equivalent to SWI/SNF complex. It has been well documented that insufficient expression of ARID1A or its function lead various carcinogenesis including that of colon cancer and breast cancer. It is interesting that these ARID1A related malignancy may be overlapped to so called metabolic-disease related cancers.
In the present study, we examined and unraveled that insufficient function of ARID1A was related to adiponectin, especially that of high molecular weight form, and T-cadherin, which is a receptor for high molecular weight adiponectin.
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| Academic Significance and Societal Importance of the Research Achievements |
ARID1A発現低下がもたらす、がん進行に対して、adiponectin補充、とくに、そのhigh molecular weight分子の補充が、必要であることをみいだした。
本研究は、いわゆるメタボリック障害が関連する癌で、adiponectinの重要性をARID1A変異発がんの観点から明らかにした。
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