E‐cadherin's role in development, tissue homeostasis and disease: Insights from mouse models
Citations Over TimeTop 10% of 2014 papers
Abstract
Recent studies uncovered critical roles of the adhesion protein E-cadherin in health and disease. Global inactivation of Cdh1, the gene encoding E-cadherin in mice, results in early embryonic lethality due to an inability to form the trophectodermal epithelium. To unravel E-cadherin's functions beyond development, numerous mouse lines with tissue-specific disruption of Cdh1 have been generated. The consequences of E-cadherin loss showed great variability depending on the tissue in question, ranging from nearly undetectable changes to a complete loss of tissue structure and function. This review focuses on these studies and discusses how they provided important insights into E-cadherin's role in cell adhesion, proliferation and differentiation, and its consequences for biological processes as epithelial-to-mesenchymal transition, vascularization, and carcinogenesis. Lastly, we present some perspectives and possible approaches for future research.
Related Papers
- → Beyond E-cadherin: roles of other cadherin superfamily members in cancer(2014)466 cited
- → E‐cadherin's role in development, tissue homeostasis and disease: Insights from mouse models(2014)61 cited
- → E-cadherin to P-cadherin switching in lobular breast cancer with tubular elements(2020)44 cited
- → Is Upregulation of BCL2 a Determinant of Tumor Development Driven by Inactivation of CDH1/E-Cadherin?(2013)9 cited
- Disordered beta-catenin expression and E-cadherin/CDH1 promoter methylation in gastric carcinoma(2006)