E-cadherin-integrin crosstalk in cancer invasion and metastasis

Marta Canel, Alan Serrels, Margaret C. Frame, Valerie G. Brunton*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)393-401
Number of pages9
JournalJournal of Cell Science
Volume126
Issue number2
DOIs
Publication statusPublished - 15 Jan 2013

Keywords

  • REGULATES E-CADHERIN
  • RHO-FAMILY GTPASES
  • E-cadherin
  • Cancer
  • CARCINOMA-CELLS
  • TYROSINE PHOSPHORYLATION
  • TUMOR PROGRESSION
  • LINKED KINASE
  • Integrins
  • ADHERENS JUNCTIONS
  • EPITHELIAL-MESENCHYMAL TRANSITION
  • Invasion
  • COLLAGEN TYPE-I
  • CELL-CELL-ADHESION

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