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Epithelial membrane protein-2 (EMP2) activates Src protein and is a novel therapeutic target for glioblastoma
Yu Qin1, Maoyong Fu2, Masamichi Takahashi3
1From the Departments of Ophthalmology and.
Abstract:
Despite recent advances in molecular classification, surgery, radiotherapy, and targeted therapies, the clinical outcome of patients with malignant brain tumors remains extremely poor. In this study, we have identified the tetraspan protein epithelial membrane protein-2 (EMP2) as a potential target for glioblastoma (GBM) killing. EMP2 had low or undetectable expression in normal brain but was highly expressed in GBM as 95% of patients showed some expression of the protein. In GBM cells, EMP2 enhanced tumor growth in vivo in part by up-regulating αvβ3 integrin surface expression, activating focal adhesion kinase and Src kinases, and promoting cell migration and invasion. Consistent with these findings, EMP2 expression significantly correlated with activated Src kinase in patient samples and promoted tumor cell invasion using intracranial mouse models. As a proof of principle to determine whether EMP2 could serve as a target for therapy, cells were treated using specific anti-EMP2 antibody reagents. These reagents were effective in killing GBM cells in vitro and in reducing tumor load in subcutaneous mouse models. These results support the role of EMP2 in the pathogenesis of GBM and suggest that anti-EMP2 treatment may be a novel therapeutic treatment.
Insights
Researchers identified epithelial membrane protein-2 (EMP2) as a promising target for glioblastoma (GBM) treatment. Targeting EMP2 with antibodies effectively killed GBM cells and reduced tumor growth, offering a potential new therapy for brain tumors.
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- Malignant brain tumors, particularly glioblastoma (GBM), have poor clinical outcomes despite advances in treatment.
- The tetraspan protein epithelial membrane protein-2 (EMP2) is highly expressed in GBM but not in normal brain tissue.
Purpose of the Study:
- To investigate the role of EMP2 in GBM pathogenesis and evaluate its potential as a therapeutic target.
- To determine if targeting EMP2 with antibodies can inhibit GBM growth and invasion.
Main Methods:
- Assessed EMP2 expression in normal brain and GBM patient samples.
- Investigated EMP2's function in GBM cells by examining its effects on integrin expression, kinase activation (FAK, Src), cell migration, and invasion in vitro and in vivo.
- Treated GBM cells and mouse models with anti-EMP2 antibodies.
Main Results:
- EMP2 is highly expressed in 95% of GBM patients, correlating with activated Src kinase.
- EMP2 promotes GBM growth, migration, and invasion by up-regulating αvβ3 integrin and activating FAK and Src kinases.
- Anti-EMP2 antibody treatment effectively killed GBM cells in vitro and reduced tumor burden in vivo.
Conclusions:
- EMP2 plays a significant role in GBM development and progression.
- Targeting EMP2 with antibody-based therapy represents a novel and promising therapeutic strategy for glioblastoma.
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