Abstract
G protein-coupled receptor 124 (GPR124; also called tumor endothelial marker 5, TEM5) is highly expressed in tumor vasculature. While recent studies have revealed a role in vasculogenesis, evidence for GPR124 function in tumor angiogenesis is lacking. Here, we demonstrate that GPR124 is required for VEGF-induced tumor angiogenesis. GPR124 silencing in human endothelial cells inhibited mouse xenograft tumor angiogenic vessel formation and tumor growth. GPR124 regulated VEGF-induced tumor angiogenic processes in vitro including cell-cell interaction, permeability, migration, invasion, and tube formation. Therefore, GPR124 plays a key role in VEGF-induced tumor angiogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 543-554 |
| Number of pages | 12 |
| Journal | Current Molecular Medicine |
| Volume | 14 |
| Issue number | 4 |
| DOIs | |
| State | Published - 2014 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Angiogenesis
- Cancer
- G protein coupled receptors (GPCR)
- Tumor
- Vascular biology
- Vascular endothelial growth factor (VEGF)
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