The International Journal of Developmental Biology

Int. J. Dev. Biol. 48: 463 - 476 (2004)

https://doi.org/10.1387/ijdb.041793ld

Vol 48, Issue 5-6

Special Issue: Invasion in Cancer and Embryonic Development

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Published: 1 September 2004

Lara D.M. Derycke and Marc E. Bracke

Laboratory of Experimental Cancerology, Department of Radiotherapy, Nuclear Medicine and Experimental Cancerology, Ghent University Hospital, Belgium.

Abstract

Cell migration is a process which is essential during embryonic development, throughout adult life and in some pathological conditions. Cadherins, and more specifically the neural cell adhesion molecule N-cadherin, play an important role in migration. In embryogenesis, N-cadherin is the key molecule during gastrulation and neural crest development. N-cadherin mediated contacts activate several pathways like Rho GTPases and function in tyrosine kinase signalling (for example via the fibroblast growth factor receptor). In cancer, cadherins control the balance between suppression and promotion of invasion. E-cadherin functions as an invasion suppressor and is downregulated in most carcinomas, while N-cadherin, as an invasion promoter, is frequently upregulated. Expression of N-cadherin in epithelial cells induces changes in morphology to a fibroblastic phenotype, rendering the cells more motile and invasive. However in some cancers, like osteosarcoma, N-cadherin may behave as a tumour suppressor. N-cadherin can have multiple functions: promoting adhesion or induction of migration dependent on the cellular context.

Keywords

N-cadherin, cancer, embryogenesis, invasion, signalling

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