Cross-talk between FGF receptor and integrin in breast cancer invasion and metastasis.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460471
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Osaka University
• Principal Investigator: Mori Seiji 大阪大学, 医学系研究科, 招へい教授 (90467506)
• Research Collaborator: TAKADA Yoshikazu University of Carifornia Davis, 教授
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: インテグリン / FGF / FGFR / 腫瘍

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.

Free Research Field

分子病理学