| Project/Area Number |
18K07263
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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 50020:Tumor diagnostics and therapeutics-related
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
椙村 春彦 浜松医科大学, 医学部, 教授 (00196742)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | がん特異的遺伝子 / 翻訳伸長反応 / スクリーニング系 / ＲNA結合蛋白質 / 癌細胞 / 癌特異的蛋白質 / 核酸医薬 / 蛋白質相互作用 / 翻訳伸長因子 / 翻訳後修飾 / 癌分子標的 / LIX1L / RNA / 癌 / 標的治療薬 |
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| Outline of Final Research Achievements |
We performed the basic research on the development of new therapeutic agents specific to LIX1L-expressing cancer by specifically inhibiting the binding between the LIX1L protein, which specifically expressed in cancer cells, and the translation elongation factor EEF1G protein.The binding of LIX1L and EEF1G is involved in the translation of proteins involved in various cancer cell proliferation, and inhibition of the binding of both proteins is effective for cancer treatment through the control of the translation of proteins required for cancer cell proliferation.
In addition, we established expression cell lines, which can analyze the binding of two proteins, LIX1L and EEF1G, on a cell base using the NanoBit system, and constructed an HTS screening system. In the future, we plan to search for candidate compounds using the compound library.
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| Academic Significance and Societal Importance of the Research Achievements |
癌特異的に発現する蛋白質LIX1Lを我々が同定し、様々な癌でLIX1L蛋白質の発現が確認されました。また、その機能解析からLIX1Lと結合する翻訳伸長因子EEF1Gとの結合が癌細胞の増殖に重要であることが明らかとなりました。以上のことから、両蛋白質の結合阻害が癌細胞における翻訳伸長反応の制御を介した新しい癌治療薬の開発に展開できると考えられます。また、候補化合物を探索するためのスクリーニング系の構築も作成しました。
今後新しい作用機序を持つ癌治療薬が癌治療の一つに選択肢として加わる可能性が推測されます。
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