| Project/Area Number |
26460471
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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, 招へい教授 (90467506)
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| Co-Investigator(Kenkyū-buntansha) |
松浦 成昭 大阪大学, 医学系研究科, 特任教授 (70190402)
河口 直正 大阪大学, 医学系研究科, 特任准教授(常勤) (70224748)
濱田 吉之輔 大阪大学, 医学系研究科, 特任准教授 (10362683)
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| Research Collaborator |
TAKADA Yoshikazu University of Carifornia Davis, 教授
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | インテグリン / FGF / FGFR / 腫瘍 / FGF受容体 / EMT |
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| Outline of Final Research Achievements |
We studied the role of αvβ3 induced by TGF-β on TGF-β-induced EMT. We elucidated that FGF1 bi-directionally regulated EMT induced by TGF-β1 in MCF10A mammary epithelial cells. TGF-β1 markedly amplified integrin αvβ3 and FGFR1. We studied if the enhancing effect of FGF1 on TGF-β1-induced EMT requires enhanced levels of both integrin αvβ3 expression and FGFR1. Knockdown of integrin β3 suppressed the enhancement by FGF1 of TGF-β1-induced EMT in MCF10A cells. Integrin-binding defective FGF1 mutant did not show bi-directional effect on TGF-β1-induced EMT in MCF10A cells. These findings suggest that enhanced integrin αvβ3 expression in addition to enhanced FGFR1 expression is critical for FGF1 to regulate TGF-β1-induced EMT in mammary epithelial cells.
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