| Project/Area Number |
21590590
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied pharmacology
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| Research Institution | Kyoto University |
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Principal Investigator |
KAMBA Tomomi 京都大学, 医学研究科, 講師 (20402836)
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| Co-Investigator(Kenkyū-buntansha) |
OGAWA Osamu 京都大学, 医学研究科, 教授 (90260611)
西山 博之 京都大学, 医学研究科, 准教授 (20324642)
兼松 明弘 京都大学, 医学研究科, 講師 (90437202)
渡部 淳 京都大学, 医学研究科, 助教 (10452335)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 腎細胞癌 / マトリックス・リモデリング / 抗血管新生療法 / VHL / JunB / MMP-2/9 / CCL2 / マトリックスリモデリング |
|---|
| Research Abstract |
The purpose of this research is to identify a pathway of the control mechanism of matrix remodeling in renal cell carcinoma and to examine whether it could be a new therapeutic target and a sensitive marker of anti-angiogenic therapy. This study indicates that the pathway of VHL-atypical PKC-JunB not through the HIF(hypoxia-inducible factor) contributes to the progression of renal cell carcinoma, and we actually confirmed with xenografts from kidney cancer cell lines that the expression of JunB affected tumor growth and angiogenesis. Moreover, we identified matrix metalloproteinase-2(MMP-2), MMP-9 and chemokine(C-C motif) ligand-2(CCL2) as downstream effectors of JunB. The results of their functional analysis suggest that they have the possibility to be new molecular targets for angiogenesis and invasion of renal cell carcinoma.
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