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

Sameh Sarray (1, 2) , Carole Siret (3) , Maxime Lehmann (3) , Naziha Marrakchi (1, 4) , José Luis (3) , Mohamed El Ayeb (1) , Frédéric André (3)

1 Institut Pasteur de Tunis
2 Faculté des Sciences
3 CRO2 - Centre de Recherches en Oncologie biologique et Oncopharmacologie
4 Faculté de Médecine de Tunis

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.

Domaines: Immunologie

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