Cell adhesion and signalling by cadherins and Ig-CAMs in cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-02

AUTHORS

Ugo Cavallaro, Gerhard Christofori

ABSTRACT

Key PointsCell-adhesion molecules of the cadherin and immunoglobulin-like cell-adhesion molecule (Ig-CAM) superfamilies not only exert their functions by mediating cell–cell and cell–matrix adhesion, but also by directly eliciting signals that are involved in tissue morphogenesis and tumour progression.In addition, signalling molecules are also able to modulate the adhesion status of the cell by acting on cell-adhesion molecules themselves, or on other components of signalling complexes.The function of epithelial (E)-cadherin is altered in most epithelial tumours during the progression to tumour malignancy. E-cadherin function can be disrupted by various genetic and epigenetic mechanisms, including modulation by signalling molecules.Loss of E-cadherin function elicits active signals that support tumour-cell migration, invasion and metastatic dissemination.In several cancer types, loss of E-cadherin function is accompanied by the gain of expression of mesenchymal cadherins, for example, neuronal (N)-cadherin and cadherin-11, in a process that is known as the cadherin switch.N-cadherin interacts with members of the fibroblast growth factor receptor (FGFR) family, thereby inducing pro-migratory and invasive signalling cascades.Neural CAM (NCAM) also associates with FGFRs. Loss of NCAM function during tumour progression affects cell–matrix adhesion through the loss of FGFR-induced, integrin-mediated cell–matrix adhesion.Several other members of the cadherin and Ig-CAM families interact with signalling molecules, thereby modulating physiological and pathological processes. More... »

PAGES

118-132

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    45 schema:description Key PointsCell-adhesion molecules of the cadherin and immunoglobulin-like cell-adhesion molecule (Ig-CAM) superfamilies not only exert their functions by mediating cell–cell and cell–matrix adhesion, but also by directly eliciting signals that are involved in tissue morphogenesis and tumour progression.In addition, signalling molecules are also able to modulate the adhesion status of the cell by acting on cell-adhesion molecules themselves, or on other components of signalling complexes.The function of epithelial (E)-cadherin is altered in most epithelial tumours during the progression to tumour malignancy. E-cadherin function can be disrupted by various genetic and epigenetic mechanisms, including modulation by signalling molecules.Loss of E-cadherin function elicits active signals that support tumour-cell migration, invasion and metastatic dissemination.In several cancer types, loss of E-cadherin function is accompanied by the gain of expression of mesenchymal cadherins, for example, neuronal (N)-cadherin and cadherin-11, in a process that is known as the cadherin switch.N-cadherin interacts with members of the fibroblast growth factor receptor (FGFR) family, thereby inducing pro-migratory and invasive signalling cascades.Neural CAM (NCAM) also associates with FGFRs. Loss of NCAM function during tumour progression affects cell–matrix adhesion through the loss of FGFR-induced, integrin-mediated cell–matrix adhesion.Several other members of the cadherin and Ig-CAM families interact with signalling molecules, thereby modulating physiological and pathological processes.
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