Abstract
INTRODUCTION: Glioblastoma multiforme (GBM) is a deadly disease with a survival of approximately 15 months. Epithelial membrane protein 2 (EMP2) is correlated with advanced disease and adverse outcomes in several cancers and has recently been found to be expressed on the surface of GBM cells. Its expression in GBM increases integrin surface expression resulting in activation of focal adhesion kinase and Src and promoting increased tumor growth, cell migration, and invasion. METHODS: Subcutaneous and orthotopic mouse models were utilized for this study. In the subcutaneous model, n = 4 BALB/c mice were inoculated with U373 cells and treated with weekly systemic treatments of either anti-EMP2 or control IgG1. Tumor size was measured weekly. In the intracranial model, n = 6 BALB/c nude mice were inoculated with U87 cells overexpressing EMP2 and treated with weekly systemic injections of either anti-EMP2 or control IgG1. Tumor size was followed with bioluminescence imaging. RESULTS: In the subcutaneous model, tumor growth was significantly reduced at 50 days when treated with anti-EMP2 antibody (19 mm3 vs. 45 mm3, p < 0.05), and the residual tumors displayed significant necrosis compared to the control group. In the intracranial model, the treatment group showed a trend toward reduced tumor growth compared to the control group. The mean fold change in average tumor radiance in the treatment group was 402 compared to 543 in the control group. CONCLUSION: Our data present an extremely novel biomarker and therapeutic target for GBM. These findings suggest that targeting EMP2 may be an effective treatment modality for GBM. Further studies are needed to fully elucidate the role of targeting EMP2 in the treatment of GBM.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.