| Project/Area Number |
23590176
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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 |
Medical pharmacy
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAMAI Ikumi 金沢大学, 薬学系, 教授 (20155237)
相沢 信 日本大学, 医学部, 教授 (30202443)
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| Co-Investigator(Renkei-kenkyūsha) |
AIZAWA Shin 日本大学, 医学部, 教授 (30202443)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 薬物動態・代謝学 / 輸送体 / 前立腺癌 / ホルモン / 去勢抵抗性 / 化学療法 / 前立腺がん / OATP / トランスポーター / がん / 幹細胞 / 白血病 |
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| Outline of Final Research Achievements |
The studied aimed to establish a role of nutrient transporter in adapted cell growth of cancer. OATP1A2 mRNA expression increased in human prostate cancer LNCaP cells under androgen-depleted condition. Knockdown of OATP1A2 mRNA in LNCaP cells resulted in loss of the DHEAS sensitivity of cell growth, colony formation and invasion capacity. Finally, the upregulation of OATP1A2 expression was also useful to deliver an OATP1A2 substrate cytostatic drug, methotrexate, to LNCaP cells, resulting in reducing their sensitivity to MTX. In summary, cell population with higher activity of OATP1A2 may be selected under androgen-depleted condition; therefore, combination therapy of complete androgen blockade with OATP1A2 substrate chemotherapeutic may be a new rationale to eradicate prostate cancer cells resistant to castration.
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