| Project/Area Number |
23592321
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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 | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHINOHARA Nobuo 北海道大学, 大学院医学研究科, 准教授 (90250422)
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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: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 腫瘍学 / 前立腺癌 / ダイオキシン受容体 / 芳香族炭化水素受容体 / アンドロゲン受容体 / Indirubin |
|---|
| Research Abstract |
The expression status of the dioxin receptor (AhR) in the cell line including the human prostate cancer was confirmed by Western blot analysis. LNCaP , which is known as prostate cancer cell line, proliferation is controlled for 3- Methylcholanthrene (3MC) and others as a typical AhR ligand, and the proliferation potency and the transcriptional ability of these ligands wereconfirmed, and androgen receptor (AR) appearance has decreased. The concentration dependency was admitted. On the other hand, the transcriptional ability of AR rose oppositely. This phenomenon was seen also in the presence or absence of androgen, and was concerned to ubiquitine- protesome system. However, it was confirmed to control both proliferation potencies and the transcriptional abilities in other ligands (ligand X). As a result, it was thought that the therapeutic gain to the hormone refractory prostate cancer was expected.
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