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Tumor endothelial markers (TEMs) that are highly expressed in human tumor vasculature compared with vasculature in normal tissue hold clear therapeutic potential. We report that the C-type lectin CLEC14A is a novel TEM. Immunohistochemical and immunofluorescence staining of tissue arrays has shown that CLEC14A is strongly expressed in tumor vasculature when compared with vessels in normal tissue. CLEC14A overexpression in tumor vessels was seen in a wide range of solid tumor types. Functional studies showed that CLEC14A induces filopodia and facilitates endothelial migration, tube formation and vascular development in zebrafish that is, CLEC14A regulates pro-angiogenic phenotypes. CLEC14A antisera inhibited cell migration and tube formation, suggesting that anti-CLEC14A antibodies may have anti-angiogenic activity. Finally, in endothelial cultures, expression of CLEC14A increased at low shear stress, and we hypothesize that low shear stress due to poor blood flow in the disorganized tumor vasculature induces expression of CLEC14A on tumor vessels and pro-angiogenic phenotypes.

Original publication

DOI

10.1038/onc.2011.233

Type

Journal article

Journal

Oncogene

Publication Date

01/2012

Volume

31

Pages

293 - 305

Addresses

Angiogenesis Group, Centre for Cardiovascular Sciences, Institute for Biomedical Research, Schools of Immunity and Infection and Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.

Keywords

Endothelium, Vascular, Cell Line, Tumor, Pseudopodia, Animals, Zebrafish, Humans, Carcinoma, Hepatocellular, Breast Neoplasms, Liver Neoplasms, Ovarian Neoplasms, Prostatic Neoplasms, Neovascularization, Pathologic, Cell Adhesion Molecules, Lectins, C-Type, Cell Movement, Female, Male, Urinary Bladder Neoplasms, Biomarkers, Tumor