Epidermal growth factor receptor is involved in enterocyte anoikis through the dismantling of E-cadherin-mediated junctions

Abstract

Pinçon-Raymond M, Cardot P, Thenet S. Epidermal growth factor receptor is involved in enterocyte anoikis through the dismantling of E-cadherin-mediated junctions.

Influence of stress on extracellular matrix and integrin biology

“…This has been described in normal epithelial and endothelial cells, whereas tumor cells are most often resistant to anoıkis (for review, see Frisch and Ruoslahti, 1997). Anoıkis may also be facilitated by the loss of cell-to-cell contacts following dissociation of the cadherin-catenin complexes (Fouquet et al, 2004;Hofmann et al, 2007;Lugo-Martinez et al, 2009). This observation strengthens the notion that anoıkis activation is a more general process for preventing inappropriate cell detachment, and, for this reason, considered as a tumor suppressor mechanism.…”

Active contractility at E-cadherin junctions and its implications for cell extrusion in cancer

“…1,10 This finding derived from the initial observation that E-cadherin clusters are found throughout junctions between cells. 1,2,11 At the apicallateral interface, clusters of E-cadherin are stabilized and concentrate in a ring-like structure that we and others have described as a zonula adherens. [12][13][14] However, extensive E-cadherin was also found distributed in clusters throughout the lateral adherens junctions (LAJ) located below the ZA.…”

Epidermal growth factor receptor signalling contributes to house dust mite-induced epithelial barrier dysfunction

“…Our results also provide insight into the underlying mechanism: HDM induces EGFR activation in a serine protease/PAR2-dependent manner, which is critical for the ensuing transient disruption of intercellular junctions. As previously described, this may involve EGFR-induced tyrosine phosphorylation and delocalisation of junctional proteins, as well as attenuated redistribution of these proteins to epithelial junctions [31][32][33][34][35]. Inhibition of EGFR reduced the disassembly of epithelial junctions and the subsequent migration/spreading, and improved the restoration of barrier function upon both HDM-induced injury and wounding.…”