Is this proven? Or is it just used as a marker to determine when a cell has undergone EMT.
E cadherin is downregulated when cells undergo EMT, and this is partially regulated transcriptionally, and by all means accelerated endocytosis might help too (I don't know if it has been proven). However, it is hard to imagine how an E cadherin could be endocytosed when it is tightly interacting with an E cadherin from the adjacent cell (i.e. an adhesion belt). It is likely that dissociation of cells is mediated by cleavage of the extracellular portion of the cadherin from the transmembrane domain and what is then left may dissociate from the protein adapter that links it to the cytoskeleton and can then be endocytosed.
I would read the following article to get an idea about the formation of extracellular soluble cadherins after cleavage from the transmembrane domain..
Tissue Barriers. 2013 Apr 1;1(2):e24783. doi: 10.4161/tisb.24783.
Cleavage of transmembrane junction proteins and their role in regulating epithelial homeostasis.
Nava P1, Kamekura R2, Nusrat A2.
Sometimes cause and effect are hard to tease apart, but try this paper:
Lysosomal Targeting of E-Cadherin: a Unique Mechanism for the Down-Regulation of Cell-Cell Adhesion during Epithelial to Mesenchymal Transitions
Felipe Palacios, Jogender S. Tushir, Yasuyuki Fujita and Crislyn D'Souza-Schorey
http://mcb.asm.org/content/25/1/389.full
Jimmy, the loss of E-cadherin is sufficient to induce the transition from adenoma to invasive carcinoma, which implies an EMT-like process (Nature. 1998 Mar 12;392(6672):190-3.; Cell. 1991 Jul 12;66(1):107-19.).However, in HCT116 cells, loss of E-cadh is not sufficient to induce N-cadh or in vitro invasion (J Cell Sci. 2010 Apr 15;123(Pt 8):1295-305. doi: 10.1242/jcs.061002. ). E-cadherin is definitely not a simple EMT marker, it is clearly an actor!
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