Tie2-expressing monocytes and tumor angiogenesis : Regulation by hypoxia and angiopoietin-2

• Published in: Cancer research (Chicago, Ill.) Vol. 67; no. 18; pp. 8429 - 8432
• Main Authors: LEWIS, Claire E, DE PALMA, Michele, NALDINI, Luigi
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15.09.2007
• Subjects: Angiopoietin-2 - biosynthesis; Angiopoietin-2 - genetics; Angiopoietin-2 - metabolism; Animals; Antineoplastic agents; Biological and medical sciences; Cell Hypoxia; Humans; Medical sciences; Monocytes - enzymology; Neoplasms - blood; Neoplasms - blood supply; Neoplasms - enzymology; Neoplasms - genetics; Neovascularization, Pathologic - blood; Neovascularization, Pathologic - enzymology; Pharmacology. Drug treatments; Receptor, TIE-2 - biosynthesis; Receptor, TIE-2 - genetics; Tumors; Up-Regulation; Tie2 receptor; Angiogenesis; Oxygen; Monocyte; Hypoxia; Angiopoietin 2; Neovascularization; Malignant tumor; Gene expression
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/0008-5472.can-07-1684

Recent findings indicate that tumor-associated macrophages are important drivers of tumor angiogenesis. Here, we review the essential role played by Tie2-expressing monocytes (TEM) in this phenomenon. TEMs are present in human blood and tumors and their elimination in various tumor models suppresses tumor angiogenesis. A ligand for Tie2, angiopoietin-2 (Ang-2), is produced by angiogenic tumor vessels and is a chemoattractant for TEMs. Hypoxia up-regulates Tie2 expression on TEMs and, together with Ang-2, down-regulates their antitumor functions. Learning more about the regulation of TEMs by the tumor microenvironment may yield new strategies to ablate the tumor vasculature.