| Project/Area Number |
26462406
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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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| Research Field |
Urology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
北川 育秀 金沢大学, 附属病院, 講師 (00452102)
角野 佳史 金沢大学, 医学系, 准教授 (10397218)
京 哲 島根大学, 医学部, 教授 (50272969)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 去勢抵抗性前立腺癌 / 再燃メカニズム / ユビキチン-プロテアソーム系 / NF-κB / 小胞体ストレス / UPR / シグナル伝達 / クロストーク |
|---|
| Outline of Final Research Achievements |
Elucidating a comprehensive mechanism through which most patients with advanced prostate cancer have an initial response to androgen deprivation therapy, but eventually progress to a castration-resistant state is critical to establish a novel treatment strategy for castration refractory prostate cancer (CRPC). We investigated the mechanism for the emersion of CRPC from the perspective of ubiquitin-proteasome system regulating both NF-kappa B and unfolded protein response (UPR) activation. Our study suggested that constitutive NF-kappa B activation and successive escape from endoplasmic reticulum stress might be one of mechanism for CRPC emersion, and that trying development of new drugs with targeting for ubiquitin-proteasome system might be a novel therapeutic strategy for the management of CRPC.
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