| Project/Area Number |
23592336
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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 | Nagasaki University |
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Principal Investigator |
TSUKASA IGAWA 長崎大学, 医歯(薬)学総合研究科, 准教授 (40295069)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Hideki 長崎大学, 大学院医歯(薬)学総合研究科, 教授 (40235122)
ONITA Toru 長崎大学, 病院, 講師 (50452850)
TAKEHARA Kousuke 長崎大学, 病院, 助教 (40580345)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 前立腺癌 / ミッドカイン / 自然炎症 / LNCaP細胞 / ﾐｯﾄﾞｶｲﾝ / PC-3細胞 |
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| Research Abstract |
In this study, we analyzed the role of midkine (MK), which is thought to have relation to homeostatic inflammation, in the progression of prostate cancer. We first evaluated the expression level of MK in the various prostate cancer cell lines. Since LNCaP cell expressed MK protein, we used this cell line for the next analysis. The changes of MK expression in LNCaP cells after treated with Dihydrotestosterone, Epidermal Growth Factor or H2O2 revealed at most 1.5 time higher protein expression than that of treatment free control cells. Although MK may have some roles in the progression of prostate cancer, e.g. cell proliferation or oxidative stress response, this independent role may not be so important. Further study is required to understand the actual role of homeostatic inflammation in prostate cancer, combined with other molecules which related to MK function.
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