2010 Fiscal Year Final Research Report
Inhibition of prostatic cancer cellular proliferation through degradation of androgen receptor by effects of dioxins
| Project/Area Number |
21791482
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Hokkaido University |
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Principal Investigator |
MARUYAMA Satoru Hokkaido University, 北海道大学病院, 助教 (80507591)
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| Project Period (FY) |
2009 – 2010
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| Keywords | ダイオキシン受容体 / 前立腺癌 / ホルモン不応性癌 / アンドロゲン受容体 |
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| 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) as a typical AhR ligand, and the proliferation potency and the transcriptional ability of these ligands were confirmed, 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. However, it was confirmed to control both proliferation potencies and the transcriptional abilities in other ligands. As a result, it was thought that the therapeutic gain to the hormone refractory prostate cancer was expected.
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