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.
Frame
Margaret C
MC
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
Inman
Gareth J
GJ
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