The cross-talk between EGFR and E-cadherin
The cross-talk between EGFR and E-cadherin
Epidermal growth factor receptor (EGFR) and adhesion protein E-cadherin are major regulators of proliferation and differentiation in epithelial cells. Consistently, defects in both EGFR and E-cadherin-mediated intercellular adhesion are linked to various malignancies. These defects in either are further exacerbated by the reciprocal interactions between the two transmembrane proteins. On the one hand, EGFR can destabilize E-cadherin adhesion by increasing E-cadherin endocytosis, modifying its interactions with cytoskeleton and decreasing its expression, thus promoting tumorigenesis. On the other hand, E-cadherin regulates EGFR localization and tunes its activity. As a result, loss and mutations of E-cadherin promote cancer cell invasion due to uncontrolled activation of EGFR, which displays enhanced surface motility and changes in endocytosis. In this minireview, we discuss the molecular and cellular mechanisms of the cross-talk between E-cadherin and EGFR, highlighting emerging evidence for the role of endocytosis in this feedback, as well as its relevance to tissue morphogenesis, homeostasis and cancer progression.
adhesion, cancer, epithelia, morphogenesis, signalling
Moreno, Miguel Ramirez
22b64166-df15-46e0-b5a5-2e99ea81d0da
Bulgakova, Natalia A.
f01bab85-42b3-403b-926c-3b56b17de5dd
20 January 2022
Moreno, Miguel Ramirez
22b64166-df15-46e0-b5a5-2e99ea81d0da
Bulgakova, Natalia A.
f01bab85-42b3-403b-926c-3b56b17de5dd
Moreno, Miguel Ramirez and Bulgakova, Natalia A.
(2022)
The cross-talk between EGFR and E-cadherin.
Frontiers in Cell and Developmental Biology, 9, [828673].
(doi:10.3389/fcell.2021.828673).
Abstract
Epidermal growth factor receptor (EGFR) and adhesion protein E-cadherin are major regulators of proliferation and differentiation in epithelial cells. Consistently, defects in both EGFR and E-cadherin-mediated intercellular adhesion are linked to various malignancies. These defects in either are further exacerbated by the reciprocal interactions between the two transmembrane proteins. On the one hand, EGFR can destabilize E-cadherin adhesion by increasing E-cadherin endocytosis, modifying its interactions with cytoskeleton and decreasing its expression, thus promoting tumorigenesis. On the other hand, E-cadherin regulates EGFR localization and tunes its activity. As a result, loss and mutations of E-cadherin promote cancer cell invasion due to uncontrolled activation of EGFR, which displays enhanced surface motility and changes in endocytosis. In this minireview, we discuss the molecular and cellular mechanisms of the cross-talk between E-cadherin and EGFR, highlighting emerging evidence for the role of endocytosis in this feedback, as well as its relevance to tissue morphogenesis, homeostasis and cancer progression.
Text
fcell-09-828673
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Accepted/In Press date: 31 December 2021
Published date: 20 January 2022
Additional Information:
Funding Information:
This work was supported by a grant from the UKRI BBSRC (BB/ P007503/1) to NB.
Keywords:
adhesion, cancer, epithelia, morphogenesis, signalling
Identifiers
Local EPrints ID: 473013
URI: http://eprints.soton.ac.uk/id/eprint/473013
ISSN: 2296-634X
PURE UUID: 43586542-81e9-4ad0-ab5b-aec977cebf58
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Date deposited: 06 Jan 2023 18:08
Last modified: 17 Mar 2024 04:15
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Author:
Miguel Ramirez Moreno
Author:
Natalia A. Bulgakova
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