| Project/Area Number |
26870703
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Medical pharmacy
Applied pharmacology
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
Niwa Satomi 京都薬科大学, 薬学部, 研究員 (90725532)
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| Research Collaborator |
NAIKI Taku 名古屋市立大学, 大学院医学研究科腎・泌尿器科学分野, 助教 (50551272)
SASAKI Shoichi 名古屋市立大学, 大学院医学研究科腎・泌尿器科学分野, 准教授 (50225869)
TAKAHASHI Satoru 名古屋市立大学, 大学院医学研究科 実験病態病理学分野, 教授 (60254281)
OHYA Susumu 京都薬科大学, 病態薬科学系 薬理学分野, 教授 (70275147)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | イオンチャネル / 前立腺癌 / KCa2.2 / Ca2+活性化K+チャネル / アンドロゲン受容体 |
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| Outline of Final Research Achievements |
Ca2+-activated K+ channels (KCa) are key molecules in cancer progression and are considered to be potential targets for cancer therapy. KCa2.2 was predominantly expressed in human prostate cancer (PCa) tissues and human PCa cell lines, LNCaP and VCaP, with higher expression levels of androgen receptor (AR). A Ca2+-activated K+ channel blocker, UCL1684 suppressed the cell proliferation through the inhibition of the store-operated Ca2+ entry (SOCE) in LNCaP cells. The anti-androgenic agents and the siRNA-mediated inhibition of AR expression downregulated the expression levels of KCa2.2 in LNCaP cells. Additionally, the expression levels of KCa2.2 was upregulated with the upregulation of AR transcripts under long-term, androgen-deficient condition, whereas it was downregulated under short-term condition. These results suggest that KCa2.2 might induce a possible candidate for novel treatment target of Castration-Resistant Prostate Cancer, CRPC.
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