| Project/Area Number |
16H05149
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
立石 敬介 東京大学, 医学部附属病院, 講師 (20396948)
前田 愼 横浜市立大学, 医学研究科, 教授 (40415956)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2016: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | 加齢 / microRNA / 細胞老化 / SASP / 癌化 / 核酸 / 老化 / non-coding RNA / 発癌 / 内科 |
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| Outline of Final Research Achievements |
To uncover the mechanisms why aging cells are prone to carcinogenesis, we focused on microRNA function during aging. Normal human derived fibroblasts produced inflammatory cytokines by aging. Especially, Interferon responsive genes were upregulated through nuclear localization of the increased levels of STATs. These phenomena happen in the non-parenchymal cells in the human liver. Thus, aging induce chronic inflammation, which imaparis the microRNA function, leading to the increased risk of carcinogenesis. Because we found that ROCK inhibitor enhances microRNA function, this compound may suppress the risk of carcinogenesis due to aging.
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| Academic Significance and Societal Importance of the Research Achievements |
加齢に伴う発癌の危険性の増加は、高齢化社会に向けて解決しなければならない課題である。本研究ではその分子機構を解析した。細胞老化に伴って炎症性サイトカインの発現が増え慢性炎症を惹起するが、それがmicroRNAの機能を減弱させ、その結果 易発癌性になることを見出した。microRNA機能を増強する化合物として見出したROCK阻害剤は、高齢に伴う発癌リスクを減らす可能性がある。
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