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

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 beta-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.
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Submitted on : Wednesday, September 21, 2011 - 3:59:02 PM
Last modification on : Tuesday, February 26, 2019 - 12:18:02 PM

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Sameh Sarray, Carole Siret, Maxime Lehmann, Naziha Marrakchi, José Luis, et al.. Lebectin increases N-cadherin-mediated adhesion through PI3K/AKT pathway.. Cancer Letters, Elsevier, 2009, 285 (2), pp.174-81. ⟨10.1016/j.canlet.2009.05.012⟩. ⟨pasteur-00621034⟩

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