N-cadherin-mediated intercellular interactions promote survival and migration of melanoma cells.
During melanoma development, loss of functional E-cadherin accompanies gain of expression of N-cadherin. The present study was carried out to investigate the functional significance of N-cadherin in melanoma cells. N-Cadherin mediated homotypic aggregation among melanoma cells as well as heterotypic adhesion of melanoma cells to dermal fibroblasts and vascular endothelial cells. Blocking of N-cadherin-mediated intercellular interaction by N-cadherin-specific antibodies increased the number of cells undergoing apoptosis. N-Cadherin- mediated cell adhesion- activated antiapoptotic protein Akt/PKB and subsequently increased beta-catenin and inactivated the proapoptotic factor BAD: Furthermore, N-cadherin promoted migration of melanocytic cells over dermal fibroblasts, suggesting that N-cadherin may also play a role in metastasis. Together, these results indicate that the cadherin subtype switching from E- to N-cadherin during melanoma development not only frees melanocytic cells from the control by keratinocytes but also provides growth and possibly metastatic advantages to melanoma cells.[1]References
- N-cadherin-mediated intercellular interactions promote survival and migration of melanoma cells. Li, G., Satyamoorthy, K., Herlyn, M. Cancer Res. (2001) [Pubmed]
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