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Identification of cellular surface markers that distinguish tumorous from normal vasculature is important for the development of tumor vessel-targeted therapy. Here, we show that Apj, a G protein-coupled receptor, is highly enriched in tumor endothelial cells but absent from most endothelial cells of adult tissues in homeostasis. By genetic targeting using Apj-CreER and Apj-DTRGFP-Luciferase, we demonstrated that hypoxia-VEGF signaling drives expansion of Apj+ tumor vessels and that targeting of these vessels, genetically and pharmacologically, remarkably inhibits tumor angiogenesis and restricts tumor growth. These in vivo findings implicate Apj+ vessels as a key driver of pathological angiogenesis and identify Apj+ endothelial cells as an important therapeutic target for the anti-angiogenic treatment of tumors.

Original publication




Journal article


Cell Rep

Publication Date





1241 - 1254.e5


Angiogenesis, Apj, anti-angiogenic treatment, surface marker, tumor therapeutic target, tumorous vessel, Aging, Animals, Apelin Receptors, Blood Vessels, Cell Hypoxia, Cell Proliferation, Endothelial Cells, Female, Human Umbilical Vein Endothelial Cells, Humans, Male, Mice, Inbred C57BL, Molecular Targeted Therapy, Neoplasms, Neovascularization, Pathologic, Signal Transduction, Tumor Hypoxia, Vascular Endothelial Growth Factor A