Inhibition of transforming growth factor-beta activity decreases angiogenesis in a human prostate cancer-reactive stroma xenograft model.
Inhibition of transforming growth factor-beta activity decreases angiogenesis in a human prostate cancer-reactive stroma xenograft model.
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发表时间：
2002-11
期刊：
影响因子：
11.2
通讯作者：
J. Tuxhorn;S. McAlhany;Feng Yang;T. Dang;D. Rowley
中科院分区：
文献类型：
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作者：
J. Tuxhorn;S. McAlhany;Feng Yang;T. Dang;D. Rowley
我们以前已经表明，反应性基质促进血管生成和生长的LNCaP人前列腺肿瘤的差异反应性基质异种移植模型。反应性间质的调节因子尚不清楚，但转化生长因子（TGF）-β 1是一个可能的候选者。在TGF-β 1潜伏相关肽（TGF-beta 1 latency-associated peptide，TGF-beta 1）或TGF-β 1中和抗体的存在下产生三向差异反应性间质肿瘤。用这两种TGF-β抑制剂治疗的肿瘤显示出血管减少，在某些区域观察到血湖。LAP处理的肿瘤的微血管密度相对于对照肿瘤降低了3.5倍。此外，与对照肿瘤相比，LAP处理的肿瘤的平均湿重减少了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。
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.