钙粘蛋白
生物
细胞生物学
成纤维细胞生长因子受体
成纤维细胞生长因子受体1
细胞粘附
细胞迁移
粘附
细胞
细胞生长
接触抑制
成纤维细胞生长因子
受体
化学
生物化学
有机化学
作者
Thao Nguyen,Laurence Duchesne,Gautham Hari Narayana Sankara Narayana,Nicole Boggetto,David G. Fernig,C.U. Murade,Benoît Ladoux,René‐Marc Mège
出处
期刊:Oncogene
[Springer Nature]
日期:2019-07-16
卷期号:38 (35): 6283-6300
被引量:20
标识
DOI:10.1038/s41388-019-0875-6
摘要
N-cadherin adhesion has been reported to enhance cancer and neuronal cell migration either by mediating actomyosin-based force transduction or initiating fibroblast growth factor receptor (FGFR)-dependent biochemical signalling. Here we show that FGFR1 reduces N-cadherin-mediated cell migration. Both proteins are co-stabilised at cell–cell contacts through direct interaction. As a consequence, cell adhesion is strengthened, limiting the migration of cells on N-cadherin. Both the inhibition of migration and the stabilisation of cell adhesions require the FGFR activity stimulated by N-cadherin engagement. FGFR1 stabilises N-cadherin at the cell membrane through a pathway involving Src and p120. Moreover, FGFR1 stimulates the anchoring of N-cadherin to actin. We found that the migratory behaviour of cells depends on an optimum balance between FGFR-regulated N-cadherin adhesion and actin dynamics. Based on these findings we propose a positive feed-back loop between N-cadherin and FGFR at adhesion sites limiting N-cadherin-based single-cell migration.
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