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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Capillary Permeability
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Cell Communication
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Cell Line
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Cell Movement / drug effects
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Cell Proliferation / drug effects
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Disease Models, Animal
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Endothelial Cells / metabolism*
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Gene Expression Regulation, Neoplastic
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Heterografts
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Humans
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Mice
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Neoplasms / genetics
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Neoplasms / metabolism*
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Neoplasms / pathology*
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Neovascularization, Pathologic / genetics
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Neovascularization, Pathologic / metabolism*
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Receptors, G-Protein-Coupled / metabolism*
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Signal Transduction / drug effects
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Vascular Endothelial Growth Factor A / pharmacology*
Substances
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ADGRA2 protein, human
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Receptors, G-Protein-Coupled
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Vascular Endothelial Growth Factor A