Development of anti-cancer strategy using IDH gene activation
| Project/Area Number |
18K07214
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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 | Okayama University of Science |
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Principal Investigator |
Kanki Keita 岡山理科大学, 生命科学部, 准教授 (10516876)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肝細胞癌 / IDH / 脱分化 / 癌悪性化 / 低酸素応答 / 悪性化 / HDAC / 低酸素シグナル / 上皮間葉系移行 |
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| Outline of Final Research Achievements |
Anti-cancer strategy using isocitrate dehydrogenase (IDH) activation was investigated in hepatocellular carcinoma (HCC) cells. IDH expression in HCC cells paralleled with a differentiation status, being downregulated during dedifferentiation induced by TGF-β signaling, Sonic hedgehog signaling and HDAC activation. Restoration of IDH expression was shown to play a role for inhibiting hypoxic response, an major cellular signaling for cancer progression, in HCC cells. Comparative study of three IDH-subtypes revealed that diverse function of these molecules in cancer cells
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では癌細胞の脱分化において発現低下するTCA回路代謝酵素の一つであるイソクエン酸脱水素酵素（IDH）に着目し、その発現賦活化により癌細胞悪性化を抑止する機構を明らかにすることを目的とした。IDHについては腫瘍学分野では癌促進作用のある変異型IDHについての研究が広く進められているが、それに比べ野生型IDHの癌細胞における働きについてはあまり知られていない。本研究で野生型IDHの低酸素応答抑制作用や、サブタイプによる違いを明らかにしたことは、IDH変異の報告のない癌種において共有される貴重な情報となる。
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Report
(5 results)
Research Products
(8 results)
