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表达Tie2的单核细胞与肿瘤血管生成:受缺氧和血管生成素-2调控

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

作者信息

Lewis Claire E, De Palma Michele, Naldini Luigi

机构信息

Tumor Targeting Group, Academic Unit of Pathology, The Sir Henry Wellcome Laboratories for Medical Research, University of Sheffield Medical School, Sheffield, United Kingdom.

出版信息

Cancer Res. 2007 Sep 15;67(18):8429-32. doi: 10.1158/0008-5472.CAN-07-1684.

Abstract

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.

摘要

最近的研究结果表明,肿瘤相关巨噬细胞是肿瘤血管生成的重要驱动因素。在此,我们综述了表达Tie2的单核细胞(TEM)在这一现象中所起的重要作用。TEM存在于人体血液和肿瘤中,在各种肿瘤模型中消除它们可抑制肿瘤血管生成。Tie2的配体血管生成素-2(Ang-2)由血管生成性肿瘤血管产生,是TEM的趋化因子。缺氧会上调TEM上的Tie2表达,并与Ang-2一起下调它们的抗肿瘤功能。更多地了解肿瘤微环境对TEM的调节可能会产生消除肿瘤血管系统的新策略。

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