肿瘤血管生成受PHD2介导的血管生成和骨髓来源细胞募集的调控。
Tumor vasculature is regulated by PHD2-mediated angiogenesis and bone marrow-derived cell recruitment.
作者信息
Chan Denise A, Kawahara Tiara L A, Sutphin Patrick D, Chang Howard Y, Chi Jen-Tsan, Giaccia Amato J
机构信息
Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.
出版信息
Cancer Cell. 2009 Jun 2;15(6):527-38. doi: 10.1016/j.ccr.2009.04.010.
Abstract
Sustained angiogenesis, through either local sprouting (angiogenesis) or the recruitment of bone marrow-derived cells (BMDCs) (vasculogenesis), is essential to the development of a tumor. How BMDCs are recruited to the tumor and their contribution to the tumor vasculature is poorly understood. Here, we demonstrate that both IL-8 and angiogenin contribute to the complementary pathways of angiogenesis and BMDC mobilization to increase tumor growth. These two factors are regulated by PHD2 in a HIF-independent but NF-kappaB-dependent manner. PHD2 levels are decreased in human cancers, compared with corresponding normal tissue, and correlate with an increase in mature blood vessels. Thus, PHD2 plays a critical role in regulating tumor angiogenesis.
摘要
持续的血管生成，无论是通过局部芽生（血管生成）还是募集骨髓来源的细胞（BMDCs）（血管发生），对于肿瘤的发展至关重要。BMDCs如何被募集到肿瘤以及它们对肿瘤血管系统的贡献尚不清楚。在这里，我们证明白细胞介素-8（IL-8）和血管生成素都有助于血管生成和BMDC动员的互补途径，以促进肿瘤生长。这两种因子由脯氨酰羟化酶2（PHD2）以不依赖缺氧诱导因子（HIF）但依赖核因子κB（NF-κB）的方式调控。与相应的正常组织相比，人类癌症中PHD2水平降低，且与成熟血管的增加相关。因此，PHD2在调节肿瘤血管生成中起关键作用。
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