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Magic roundabout, a tumor endothelial marker: expression and signaling
Pankaj Seth1, Yanfeng Lin, Jun-ichi Hanai
1Renal Division and Center for Study of the Tumor Microenvironment, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Biochemical and Biophysical Research Communications
|May 17, 2005
Summary
Magic roundabout (MRB) is overexpressed in tumor endothelial cells and inhibits their migration. This finding suggests MRB plays a role in regulating endothelial cell migration during tumor angiogenesis.
Area of Science:
- Molecular biology
- Cell biology
- Oncology
Background:
- Molecular signals guiding blood vessels are not fully understood but resemble neuronal guidance cues.
- These cues are vital for normal blood vessel development and crucial in tumor angiogenesis.
Purpose of the Study:
- To investigate the role of the Robo family member, magic roundabout (MRB), in tumor angiogenesis.
- To characterize MRB's function in endothelial cell migration and identify its signaling pathway.
Main Methods:
- Examined MRB expression in tumor versus normal endothelial cells.
- Assessed MRB's effect on endothelial cell migration, with and without Slit2 stimulation.
- Investigated the involvement of the Ras-Raf-Mek-Erk pathway in MRB-mediated inhibition.
Main Results:
- MRB is differentially overexpressed in tumor endothelial cells across various solid tumors.
- MRB activation, ligand-independent or via Slit2, inhibits VEGF and FGF-induced endothelial cell migration.
- MRB-induced inhibition of migration is partially mediated by the Ras-Raf-Mek-Erk pathway.
Conclusions:
- MRB is a tumor endothelial-specific molecule.
- MRB expression and activation can inhibit endothelial cell migration.
- MRB is hypothesized to regulate endothelial cell migration in tumor angiogenesis.