| Project/Area Number |
23590446
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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 |
Experimental pathology
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| Research Institution | Osaka University |
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Principal Investigator |
MORI Seiji 大阪大学, 医学(系)研究科(研究院), 助教 (90467506)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUURA Nariaki 大阪大学, 大学院医学系研究科, 教授 (70190402)
KAWAGUCHI Naomasa 大阪大学, 大学院医学系研究科, 準教授 (70224748)
HAMADA Yoshinosuke 大阪大学, 大学院医学系研究科, 特任助教 (10362683)
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| Research Collaborator |
TAKADA Yoshikazu University of Carifornia Davis, 教授
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | インテグリン / FGF / FGF受容体 / 血管新生 |
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| Research Abstract |
We previously reported that Fibroblast growth factor 1 (FGF1) binds both FGF receptor and integrin avb3, and also reported that integrin binding defective FGF1 mutant (Arg 50 to Glu, R50E) is defective in a fibroblast cell proliferation and migration. In this study, we tested if the interaction between FGF1 and integrin avb3 is required for angiogenesis and tumor growth. Here we demonstrated that FGF1-R50E is defective in inducing endothelial cell migration and tube formation, and suppressed wild-type FGF1-induced signaling (dominant-negative effect) in vitro. FGF1-R50E suppressed growth of colon cancer cells which subcutaneously transplanted in nude mice. These findings suggest that FGFR and integrin avb3 crosstalk through direct integrin binding to FGF, and that R50E acts as an antagonist to FGFR. We proposed that FGF1-R50E has potential as an anti-angiogenesis and anti-cancer therapeutic.
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