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Isolation and Culture Expansion of Tumor-specific Endothelial Cells
10:15

Isolation and Culture Expansion of Tumor-specific Endothelial Cells

Published on: October 14, 2015

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
PubMed

Insights

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.

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