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Paper Description


Lebectin increases N-cadherin-mediated adhesion through PI3K/AKT pathway


Authors: Sameh SARRAY, Carole Siret, Maxime Lehmann, Naziha Marrakchi, José Luis, Mohamed El Ayeb, and Frédéric André
Abstract: Cell adhesion molecules, including cadherins and integrins, play an essential role during tumor progression and represent potential targets for the development of new therapeutic agents. We previously showed that lebectin, a C-type lectin protein (CLP) issued from Macrovipera lebectina snake venom, inhibits integrin-mediated migration of IGR39 melanoma cells. Here we assessed whether lebectin modulates cell–cell adhesion. We demonstrated that lebectin promotes N-cadherin/catenin complex reorganization at cell–cell contacts, inducing a strengthening of intercellular adhesion. This reorganization is associated to phosphorylation of b-catenin on tyrosine 142 residue. Interestingly, lebectin acts on N-cadherin-mediated cell–cell contacts through PI3K/Akt pathway. This effect could contribute to the blockage of tumor cell migration previously observed.
Published in: Cancer letters;285():174-181
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