E-Cadherin in Pancreatic Ductal Adenocarcinoma: A Multifaceted Actor during EMT
Open Access
- 21 April 2020
- Vol. 9 (4), 1040
- https://doi.org/10.3390/cells9041040
Abstract
Epithelial-to-mesenchymal transition (EMT) is a step-wise process observed in normal and tumor cells leading to a switch from epithelial to mesenchymal phenotype. In tumors, EMT provides cancer cells with a metastatic phenotype characterized by E-cadherin down-regulation, cytoskeleton reorganization, motile and invasive potential. E-cadherin down-regulation is known as a key event during EMT. However, E-cadherin expression can be influenced by the different experimental settings and environmental stimuli so that the paradigm of EMT based on the loss of E-cadherin determining tumor cell behavior and fate often becomes an open question. In this review, we aimed at focusing on some critical points in order to improve the knowledge of the dynamic role of epithelial cells plasticity in EMT and, specifically, address the role of E-cadherin as a marker for the EMT axis.Keywords
This publication has 165 references indexed in Scilit:
- Prognostic Significance of Twist and N-Cadherin Expression in NSCLCPLOS ONE, 2013
- E‐cadherin interactions are required for Langerhans cell differentiationEuropean Journal of Immunology, 2012
- Loss of E-cadherin expression and outcome among patients with resectable pancreatic adenocarcinomasLaboratory Investigation, 2011
- Metastatic Progression of Prostate Cancer and E-CadherinThe American Journal of Pathology, 2011
- Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor ProgressionJournal of Mammary Gland Biology and Neoplasia, 2010
- E-Cadherin Marks a Subset of Inflammatory Dendritic Cells that Promote T Cell-Mediated ColitisImmunity, 2010
- Epithelial-Mesenchymal Transitions in Development and DiseaseCell, 2009
- KLRG1—more than a marker for T cell senescenceAGE, 2009
- Chapter 10 The Cancer Cell–Leukocyte Fusion Theory of MetastasisAdvances in Cancer Research, 2008
- Disruption of E-Cadherin-Mediated Adhesion Induces a Functionally Distinct Pathway of Dendritic Cell MaturationImmunity, 2007