Decoding the mechanisms of cancer cell growth
| Project/Area Number |
18H02681
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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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| Review Section |
Basic Section 50010:Tumor biology-related
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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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 |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2019: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2018: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | カルシニューリン / サイクリンD1 / タンパク分解 / プロリン異性化酵素 / アンドロゲン受容体 / DNA損傷 / Chk1 / シグナル伝達 / がん / 乳癌 / FK506 / 細胞周期 / チェックポイント |
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| Outline of Final Research Achievements |
The calcineurin/NFAT (nuclear factor of activated T cells) pathway plays an essential role in carcinogenesis and metastatic potential of breast cancer. However, the molecular mechanism of the antiproliferative effect of calcineurin inhibition is unknown. We have found that calcineurin inhibition delays cell cycle progression in G1/S and promotes cyclin D1 degradation by inhibiting dephosphorylation of Thr286. Overexpression of cyclin D1 partially rescued the delayed progression of G1/S, indicating that cyclin D1 is an important factor downstream of calcineurin inhibition.
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| Academic Significance and Societal Importance of the Research Achievements |
カルシニューリンがサイクリンD1の転写に重要であることが報告されているが、本研究成果からカルシニューリンがサイクリンD1を脱リン酸化し、タンパク分解を阻害することが明らかとなった。トリプルネガティブ乳がんで高活性化しているカルシニューリンを阻害すると、サイクリンD1の発現低下、細胞増殖を抑制できる。トリプルネガティブ乳がんの新たな治療薬の開発に繋げていくことが今後の課題である。
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Report
(4 results)
Research Products
(17 results)
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[Journal Article] Cdk1-mediated DIAPH1 phosphorylation maintains metaphase cortical tension and inactivates the spindle assembly checkpoint at anaphase.2019
Author(s)
Nishimura K, Johmura Y, Deguchi K, Jiang Z, Uchida KSK, Suzuki N, Shimada M, Chiba Y, Hirota T, Yoshimura SH, Kono K, Nakanishi M.
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Journal Title
Nature Communications
Volume: 10
Issue: 1
Pages: 1-10
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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