| Project/Area Number |
18K16724
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 56030:Urology-related
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| Research Institution | Chiba University |
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Principal Investigator |
KATO MAYUKO 千葉大学, 医学部附属病院, 助教 (80733857)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | マイクロRNA / 去勢抵抗性前立腺癌 |
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| Outline of Final Research Achievements |
MicroRNA expression profiles were prepared based on autopsy specimens of metastatic castration-resistant prostate cancer. When miR -199a/b -3p was introduced into a prostate cancer cell line, its ability to proliferate, migrate, and invade was inhibited. The increased expression of NCAPH (condensin I complex subunit H) was directly regulated by miR -199a/b -3p. In a public database analysis, elevated NCAPH expression was significantly associated with shorter disease-free survival. NCAPH is upregulated in hormone-sensitive and castration-resistant prostate cancer specimens, and knockdown of NCAPH significantly inhibited migration and invasion.
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| Academic Significance and Societal Importance of the Research Achievements |
転移を生じた薬剤耐性腫瘍細胞に対する新しい治療法の開発は非常に重要である。今回、エンザルタミド、アビラテロン、カバジタキセル治療後の剖検検体を使用して、転移性去勢抵抗性前立腺癌(mCRPC)マイクロRNA発現プロファイルを作成した。アンドロゲン非依存性となった前立腺癌細胞において、治療抵抗性や遠隔転移の分子メカニズムを解明することは、CRPCに対する新たな診断マーカーや治療戦略の開発において画期的な進歩をもたらす。
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