Cooperative expression of junctional adhesion molecule-C and -B supports growth and invasion of glioma.

摘要: Brain invasion is a biological hallmark of glioma that contributes to its aggressiveness and limits the potential surgery irradiation. Deregulated expression adhesion molecules on cells thought contribute this process. Junctional (JAMs) include several IgSF members involved in leukocyte trafficking, angiogenesis, cell polarity. They are expressed mainly by endothelial cells, white blood platelets. Here, we report JAM-C human gliomas, but not their normal cellular counterpart. This correlates with genes cytoskeleton remodeling migration. These genes, identified transcriptomic approach, poliovirus receptor cystein-rich 61, both known promote invasion, as well actin filament associated protein, c-Src binding partner. Gliomas also aberrantly express JAM-B, high affinity ligand. Their interaction activates proto-oncogene, central upstream molecule pathways regulating migration invasion. In tumor microenvironment, co-expression may thus through paracrine stimuli from cells. Accordingly, JAM-C/B blocking antibodies impair vivo growth highlighting JAM-B new targets for treatment gliomas.