| Project/Area Number |
24791658
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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 |
Urology
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| Research Institution | Nagoya City University |
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Principal Investigator |
NAIKI Taku 名古屋市立大学, 医学(系)研究科(研究院), 研究員 (50551272)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 去勢抵抗性前立腺癌 / 酸化ストレス / Glutathione peroxidase 2 / 動物モデル / 前立腺癌 / 去勢抵抗性 / 遺伝子治療 |
|---|
| Research Abstract |
Prostate cancer generally acquires castration-resistant growth capacity with progression, resulting in resistance to anti-androgen therapy. Therefore, identification of genes that are regulated through this process may be important. We previously established a new castration-resistant prostate cancer (CRPC) metastatic model. We found that the glutathione peroxidase 2 (GPX2) gene was overexpressed in CRPC model, and we presented novel data showing that silencing of GPX2 by siRNA caused significant growth inhibition, and increased intracellular ROS in CRPC. Analyses of prostatectomy specimens demonstrated that GPX2 expression was significantly higher in residual cancer foci after hormone therapy than in hormone naive cancer foci. Moreover, patients with highly expressed GPX2 in biopsy specimen had significantly lower prostate-specific antigen recurrence-free survival and overall survival than those negative for GPX2. These findings suggest that GPX2 may be therapeutic target for CRPC.
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