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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

DOI

10.1016/j.celrep.2018.10.015

Type

Journal article

Journal

Cell Rep

Publication Date

30/10/2018

Volume

25

Pages

1241 - 1254.e5

Keywords

Angiogenesis, Apj, anti-angiogenic treatment, surface marker, tumor therapeutic target, tumorous vessel