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- W2002603913 endingPage "401" @default.
- W2002603913 startingPage "393" @default.
- W2002603913 abstract "E-cadherin is a single-pass transmembrane protein that mediates homophilic cell-cell interactions. Tumour progression is often associated with the loss of E-cadherin function and the transition to a more motile and invasive phenotype. This requires the coordinated regulation of both E-cadherin-mediated cell-cell adhesions and integrin-mediated adhesions that contact the surrounding extracellular matrix (ECM). Regulation of both types of adhesion is dynamic as cells respond to external cues from the tumour microenvironment that regulate polarity, directional migration and invasion. Here, we review the mechanisms by which tumour cells control the cross-regulation between dynamic E-cadherin-mediated cell-cell adhesions and integrin-mediated cell-matrix contacts, which govern the invasive and metastatic potential of tumours. In particular, we will discuss the role of the adhesion-linked kinases Src, focal adhesion kinase (FAK) and integrin-linked kinase (ILK), and the Rho family of GTPases." @default.
- W2002603913 created "2016-06-24" @default.
- W2002603913 creator A5001264667 @default.
- W2002603913 creator A5011548408 @default.
- W2002603913 creator A5036498449 @default.
- W2002603913 creator A5089581432 @default.
- W2002603913 date "2013-01-15" @default.
- W2002603913 modified "2023-10-14" @default.
- W2002603913 title "E-cadherin–integrin crosstalk in cancer invasion and metastasis" @default.
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