| Project/Area Number |
25861410
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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 | Gunma University |
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Principal Investigator |
YOSHITAKA Sekine 群馬大学, 医学(系)研究科(研究院), 助教 (00516370)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 前立腺癌 / スタチン / AKR1C3 / NSAIDs |
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| Outline of Final Research Achievements |
Statins have biological activities which inhibit prostate cancer (PC) growth. However, the exact mechanisms are still unclear. In this study, we and investigated the effects of statins on expressions of enzymes for steroid synthesis in androgen independent PC cells. After treatment of Simvastatin (Sim), there are significant alterations in expressions of enzymes for de novo steroid synthesis pathways. Especially, the expression of AKR1C3 increased more than 50 times in PC-3. Knockdown of AKR1C3 by siRNA increased Sim-induce inhibitions of cell proliferation and migration in PC-3. Similarly, the combination Sim with meclofenamic acid (MA), which inhibits AKR1C3, increased simvastatin-induce inhibitions of cell proliferation and migration in PC-3. Sim altered some gene expressions of enzymes for de novo steroid synthesis pathway in PC cells. Moreover, MA was found to have a possible role in modulating cancer progression via inhibit AKR1C3 by the combination use of Sim.
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