NCAM is at the heart of reciprocal regulation of E-cadherin- and integrin-mediated adhesions via signaling modulation.
New work by Lehembre et al. in The EMBO Journal reveals that the cell-adhesion molecule, NCAM, is at the heart of crosstalk between E-cadherin loss and reciprocal focal adhesion assembly during the epithelial to mesenchymal transition (EMT). NCAM upregulation induces the formation of novel signaling complexes that correlate with NCAM-dependent focal adhesion assembly, migration, and cancer cell invasion.
Edinburgh Cancer Research Centre, Institute of Genetics and Molecular Medicine, Western General Hospital, Crewe Road South, Edinburgh EH4 2XR, United Kingdom. m.frame@ed.ac.uk
Margaret C
MC
Frame
Gareth J
GJ
Inman
D000818:Animals; D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D022001:Focal Adhesions / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D019006:Neural Cell Adhesion Molecules / Q000378:metabolism*; D015398:Signal Transduction
D015820:Cadherins; D016023:Integrins; D019006:Neural Cell Adhesion Molecules