Quantitative analysis of gene expressions of vascular endothelial growth factor-related factors and their receptors in renal cell carcinoma
Quantitative analysis of gene expressions of vascular endothelial growth factor-related factors and their receptors in renal cell carcinoma
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DOI：
10.1620/tjem.195.101
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发表时间：
2001-10-01
影响因子：
2.2
通讯作者：
Kato, T
中科院分区：
文献类型：
--
作者：
Tsuchiya, N;Sato, K;Kato, T
血管内皮生长因子（VEGF）相关因子被认为调节血管生成，这是实体肿瘤生长中的重要事件。本研究旨在探讨VEGF相关因子基因（VEGF、VEGF-B和VEGF-C）及其受体基因（VEGFR-1和VEGFR-2）在肾细胞癌（RCC）中的表达。肾癌组织中VEGF、VEGFR-1和VEGFR-2的表达水平与相应正常肾组织相比差异有统计学意义。肿瘤组织中VEGF的表达水平与VEGFR-1、VEGFR-2的表达水平显著相关。VEGF-B、VEGF-C基因在肾细胞癌和正常肾组织中的表达无显著性差异。在肿瘤细胞和内皮细胞中观察到VEGF、VEGFR-1和VEGFR-2的中度至高度蛋白表达，而VEGF-B和VEGF-C的蛋白表达较低。提示VEGF及其受体VEGFR-1、VEGFR-2在肾细胞癌血管生成中起重要作用，而VEGF-B、VEGFR-C在肾细胞癌血管生成中可能不起作用。此外，由于VEGFR-1和VEGFR-2蛋白在肿瘤细胞和内皮细胞中表达，这些受体也可能与RCC的进展有关。(C)东北大学医学出版社。
Vascular endothelial growth factor (VEGF)-related factors are believed to regulate angiogenesis, an essential event in the growth of solid tumors. In this study, we investigated the expression of VEGF-related factor genes (VEGF, VEGF-B, and VEGF-C) and their receptor genes (VEGFR-1 and VEGFR-2) in renal cell carcinoma (RCC). There were significant differences in the expression level of VEGF, VEGFR-1 and VEGFR-2 between RCC and the corresponding normal renal tissue. The expression level of VEGF in the tumor tissue significantly correlated with those of VEGFR-1 and VEGFR-2. Expression levels VEGF-B and VEGF-C genes were not significantly different between RCC and normal renal tissue. A moderate to high protein expression for VEGF, VEGFR-1, and VEGFR-2 was observed in both the tumor cells and the endothelial cells, whereas the protein expression was low for VEGF-B and VEGF-C. The present results suggested that VEGF and its receptors VEGFR-1 and VEGFR-2 cooperates to play a crucial role in the angiogenesis of RCC, while VEGF-B and VEGFR-C may not. Furthermore, since VEGFR-1 and VEGFR-2 proteins were expressed in the tumor cells as well as in the endothelial cells, these receptors may also be responsible for the progression of RCC. (C) 2001 Tohoku University Medical Press.