Both the structure and sequence of E-Cadherin are similar with those of N-Cadherin. However the function of these two cadherins is totally different. Why?
Well, it depends on what you intend as "totally different". In fact, E- and N-cadherins share similar molecular functions: they form homophilic interactions with same molecules on other cells, thus allowing cell-cell interaction; they are anchored to the microfilaments thanks to the catenins, allowing mechanical coupling of the cytoskeletons of two contiguous cells; they are constituents of the Adherens Junction. That said, they are expressed by different kind of cells and tissues during embryonic development and adult life, so that only tissues that express a particular cadherin are affected by its genetic inactivation. In other words: E-cadherin is different from N-cadherin primarily because they are expressed by different tissues.
Well, it depends on what you intend as "totally different". In fact, E- and N-cadherins share similar molecular functions: they form homophilic interactions with same molecules on other cells, thus allowing cell-cell interaction; they are anchored to the microfilaments thanks to the catenins, allowing mechanical coupling of the cytoskeletons of two contiguous cells; they are constituents of the Adherens Junction. That said, they are expressed by different kind of cells and tissues during embryonic development and adult life, so that only tissues that express a particular cadherin are affected by its genetic inactivation. In other words: E-cadherin is different from N-cadherin primarily because they are expressed by different tissues.
Thank you very much for you answer. however what I am confused is that E-Cadherin plays reverse roles in EMT compared with N-Cadherin. So the mechanism is not explained.
OK, now I understand your point better. Basically, during the EMT process E-cadherin expression is switched off and N-cadherin is switched on. In mesenchymal cells, N-cadherin mediates adhesion (it is required for collective cell migration), but is not sufficient by itself to promote the acquisition of epithelial features. This is not because of an innate difference between E-cadherin and N-cadherin, as N-cadherin is involved in cell adhesion in many epithelia, like those of biliary ducts, renal tubules, and epidiymis. The difference instead rely on the lack of additional epithelial junctional and polarity molecules in mesenchymal cells; these molecules work together with cadherins to sustain the epithelial phenotype. Loss of E-cadherin is indeed one of the many events that occur during EMT, but it is not sufficient per se to lead cells losing their epithelial phenotype; conversely, gain of N-cadherin does not lead mesenchymal cells to acquire an epithelial phenotype, unless other epithelial junctional and polarity molecules are reactivated.
So would it be fair to say that E-cadherins and N-cadherins perform nearly equivalent roles in cell fusion? I am looking at fusion of myoblasts, and the literature implicates N-cadherins in the process, but E-cadherins seem not to be. Are E-cadherins present in myoblasts as a progenitor of fusion, or is N-cadherin the "equivalent" of E-cadherin in myoblasts? Thank you!
How E cadherin and N cadherin affect metastasis in breast cancer through Kiss peptin?
Epithelial-mesenchymal transition (EMT) leads to the formation of mesenchymal cells. It is marked by decreased expression of E-cadherin and upregulation of N-cadherin, which promotes cell migration (PMID: 23481201). Similarly, upregulation of N-cadherin is observed in many cancer cell types and is associated with increased invasiveness and metastasis.
In EMT, E-cadherin downregulate but N-cadherin upregulate
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