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© K. Melican.
Human microvessel (red) colonized by N. meningitidis (green).
Publication : Oncogene

Enhanced cell-cell contact stability and decreased N-cadherin-mediated migration upon fibroblast growth factor receptor-N-cadherin cross talk.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Oncogene - 01 Aug 2019

Nguyen T, Duchesne L, Sankara Narayana GHN, Boggetto N, Fernig DD, Uttamrao Murade C, Ladoux B, Mège RM,

Link to Pubmed [PMID] – 31312021

Link to DOI – 10.1038/s41388-019-0875-6

Oncogene 2019 08; 38(35): 6283-6300

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.

https://pubmed.ncbi.nlm.nih.gov/31312021