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

详细信息    查看全文

• 作者：Sameh Sarray ; Carole Siret ; Maxime Lehmann ; Naziha Marrakchi ; José ; Luis ; Mohamed El Ayeb ; Fré ; dé ; ric André
• 关键词：Cell– ; cell adhesion ; C type lectin protein ; Cancer ; Snake venom
• 刊名：Cancer Letters
• 出版年：2009
• 出版时间：28 November 2009
• 年：2009
• 卷：285
• 期：2
• 页码：174-181
• 全文大小：996 K

文摘

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 β-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.