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Targeting netrin-1/DCC interaction in diffuse large B-cell and mantle cell lymphomas

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Broutier, Laura | Creveaux, Marion | Vial, Jonathan | Tortereau, Antonin | Delcros, Jean-Guy | Chazot, Guillaume | Mccarron, Mark J | Léon, Sophie | Pangault, Céline | Gadot, Nicolas | Colombe, Amélie | Boulland, Marie-Laure | Blachier, Jonathan | Marie, Julien C | Traverse-Glehen, Alexandra | Donzé, Olivier | Chassagne-Clement, Catherine | Salles, Gilles | Tarte, Karin | Mehlen, Patrick | Castets, Marie

Edité par CCSD ; Wiley Open Access -

International audience. DCC (Deleted in Colorectal Carcinoma) has been demonstrated to constrain tumor progression by inducing apoptosis unless engaged by its ligand netrin-1. This has been shown in breast and colorectal cancers; however, this tumor suppressive function in other cancers is not established. Using a transgenic mouse model, we report here that inhibition of DCC-induced apoptosis is associated with lymphomagenesis. In human diffuse large B-cell lymphoma (DLBCL), an imbalance of the netrin-1/DCC ratio suggests a loss of DCC-induced apoptosis, either via a decrease in DCC expression in germinal center subtype or by up-regulation of netrin-1 in activated B-cell (ABC) one. Such imbalance is also observed in mantle cell lymphoma (MCL). Using a netrin-1 interfering antibody, we demonstrate both in vitro and in vivo that netrin-1 acts as a survival factor for ABC-DLBCL and MCL tumor cells. Together, these data suggest that interference with the netrin-1/DCC interaction could represent a promising therapeutic strategy in netrin-1-positive DLBCL and MCL

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