Tuxhorn Jennifer A, McAlhany Stephanie J, Yang Feng, Dang Truong D, Rowley David R
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Cancer Res. 2002 Nov 1;62(21):6021-5.
We have shown previously that reactive stroma promotes angiogenesis and growth of LNCaP human prostate tumors in the differential reactive stroma xenograft model. Regulators of reactive stroma are not known, but transforming growth factor (TGF)-beta1 is a likely candidate. Three-way differential reactive stroma tumors were generated in the presence of TGF-beta1 latency-associated peptide (LAP) or TGF-beta1 neutralizing antibody. Tumors treated with either of those TGF-beta inhibitors exhibited a reduction in blood vessels, and blood lakes were observed in some areas. The microvessel density of LAP-treated tumors was decreased 3.5-fold relative to control tumors. Moreover, the average wet-weight of LAP-treated tumors was reduced 46% compared with control tumors. The results of this study suggest that TGF-beta regulates reactive stroma and its ability to promote angiogenesis and tumor growth.
我们之前已经表明，在差异反应性基质异种移植模型中，反应性基质可促进LNCaP人前列腺肿瘤的血管生成和生长。反应性基质的调节因子尚不清楚，但转化生长因子（TGF）-β1可能是一个候选因子。在存在TGF-β1潜伏相关肽（LAP）或TGF-β1中和抗体的情况下，生成了三向差异反应性基质肿瘤。用这两种TGF抑制剂之一处理的肿瘤显示血管减少，并且在一些区域观察到血湖。与对照肿瘤相比，LAP处理的肿瘤的微血管密度降低了3.5倍。此外，与对照肿瘤相比，LAP处理的肿瘤的平均湿重降低了46％。这项研究的结果表明，TGF-β调节反应性基质及其促进血管生成和肿瘤生长的能力。
