Project/Area Number |
24890230
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Urology
|
Research Institution | Keio University |
Principal Investigator |
TAKEO Kosaka 慶應義塾大学, 医学部, 助教 (30445407)
|
Project Period (FY) |
2012-08-31 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 前立腺癌 / 血管新生 / アンドロゲン / 去勢抵抗性前立腺癌 / 微小環境 / VASH1 / C4-2AT6 / 薬剤耐性 / 5α還元酵素 / 去勢抵抗性 |
Research Abstract |
To reveal tumor microenvironment in Prostate Cancer (PCa), we focused on angiogenesis and androgen production. We examine the expression of VASH1 in PCa specimens. We found VASH1 density represents a clinically relevant predictor of patient prognosis and can be a new biomarker that would provide additional prognostic information in PCa (Kosaka T. et al. Br J Cancer 2013). To ascertain the potential SRD5A activity, we cultured two human CRPC cell lines: C4-2 and C4-2AT6 cells with steroid precursors: 13C-Adione, and analyzed the sequential biosynthesis of 13C-T and 13C-DHT by LC/MS/MS. 13C-DHT concentration in C4-2AT6 cells was significantly lower than C4-2. An increased concentration of DHT did not have a positive effect on cell proliferation. SRD5A inhibitors did not have any inhibitory effect, suggesting CRPC cells may have an unknown regulation system to protect themselves from androgenic suppressive effect mediated by SRD5A activity (Kosaka T. et al. Scientific Rep 2013).
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