The Autophagic Route of E-Cadherin and Cell Adhesion Molecules in Cancer Progression.
Manuela SantarosaRoberta MaestroPublished in: Cancers (2021)
Cell-to-cell adhesion is a key element in epithelial tissue integrity and homeostasis during embryogenesis, response to damage, and differentiation. Loss of cell adhesion and gain of mesenchymal features, a phenomenon known as epithelial to mesenchymal transition (EMT), are essential steps in cancer progression. Interestingly, downregulation or degradation by endocytosis of epithelial adhesion molecules (e.g., E-cadherin) associates with EMT and promotes cell migration. Autophagy is a physiological intracellular degradation and recycling process. In cancer, it is thought to exert a tumor suppressive role in the early phases of cell transformation but, once cells have gained a fully transformed phenotype, autophagy may fuel malignant progression by promoting EMT and conferring drug resistance. In this review, we discuss the crosstalk between autophagy, EMT, and turnover of epithelial cell adhesion molecules, with particular attention to E-cadherin.
Keyphrases
- cell adhesion
- cell death
- epithelial mesenchymal transition
- papillary thyroid
- signaling pathway
- cell migration
- oxidative stress
- endoplasmic reticulum stress
- induced apoptosis
- squamous cell
- single cell
- stem cells
- cell cycle arrest
- cell therapy
- bone marrow
- lymph node metastasis
- mesenchymal stem cells
- young adults
- pseudomonas aeruginosa
- escherichia coli
- staphylococcus aureus
- reactive oxygen species
- bone mineral density