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CD155/PVR Enhances Glioma Cell Dispersal by Regulating Adhesion Signaling and Focal Adhesion Dynamics

¹ Department of Physiology, Tufts University School of Medicine, Boston, Massachusetts and ² Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut

Requests for reprints: Daniel G. Jay, Department of Physiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111. Phone: 617-636-6714; Fax: 617-636-0445; E-mail: daniel.jay{at}tufts.edu.

We recently identified the immunoglobulin-CAM CD155/PVR (the poliovirus receptor) as a regulator of cancer invasiveness and glioma migration, but the mechanism through which CD155/PVR controls these processes is unknown. Here, we show that expression of CD155/PVR in rat glioma cells that normally lack this protein enhances their dispersal both in vitro and on primary brain tissue. CD155/PVR expression also reduced substrate adhesion, cell spreading, focal adhesion density, and the number of actin stress fibers in a substrate-dependent manner. Furthermore, we found that expression of CD155/PVR increased Src/focal adhesion kinase signaling in a substrate-dependent manner, enhancing the adhesion-induced activation of paxillin and p130Cas in cells adhering to vitronectin. Conversely, depletion of endogenous CD155/PVR from human glioma cells inhibited their migration, increased cell spreading, and down-regulated the same signaling pathway. These findings implicate CD155/PVR as a regulator of adhesion signaling and suggest a pathway through which glioma and other cancer cells may acquire a dispersive phenotype.

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