期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.828673
关键词
adhesion; morphogenesis; cancer; signalling; epithelia
资金
- UKRI BBSRC [BB/P007503/1]
- BBSRC [BB/P007503/1] Funding Source: UKRI
EGFR and E-cadherin are major regulators of proliferation and differentiation in epithelial cells, and defects in either can lead to malignancies. The reciprocal interactions between EGFR and E-cadherin contribute to tumorigenesis and cancer cell invasion through modulation of adhesion and activity regulation. Understanding the crosstalk between EGFR and E-cadherin is important for tissue morphogenesis, homeostasis, and cancer progression.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据