Analysis of key angiogenic factors to emphasize the impact of endostatin

我们建立了内皮抑素的转染系统，显示了抗血管生成和抑制肿瘤生长的作用。然而，这种效果并没有维持很长一段时间。最后，转内皮抑素的动物死亡，没有肿瘤休眠。也没有关于有效的临床试验的报道。我们推测内皮抑素的短期作用依赖于某些血管生成因子的上调。在本研究中，我们将内皮抑素基因导入小鼠肺，并分析了血管内皮生长因子基因的表达。采用定量RT-PCR法，以GAPDHmRNA为内对照，定量检测血管内皮细胞生长因子的表达。肺组织中均有内皮抑素和血管内皮生长因子的表达，转染组(n=6)的表达高于对照组(n=6)(方差分析Schffe‘s法p=0.0755，Mann-Whitney U检验p=0.055)。这一机制尚不清楚，但数据非常重要。这可能提示抑制血管内皮生长因子可延长内皮抑素的作用。下一步，我们可以尝试内皮抑素基因转导，同时抑制血管内皮生长因子，以证明目前的数据，实现肿瘤的休眠。

We have established the endostatin transfection systems which showed the impact of antiangiogenesis and suppression of tumor growth. However the effect was not maintained for a long time. Finally the endostatin-tranfected animals died without tumor dormancy. There, also, have been no reports of effective clinical trials. We hypothesized the reasons he short effect of endostatin depended on up-regulation of some kinds of angiogenic factors. In the present study we have transfected mice lungs with endostatin gene and analyzed the VEGF gene expression. We used quantitative RT-PCR method to quantify the VEGF mRNA using GAPDH mRNA as an internal control. The both expression of Endostatin and VEGF mRNAs in the lung were apparent and the expression of VEGF mRNA in trasfection group (n=6) was higher than in cntol group (n=6) (p=0.0755 in Schffe's method in ANOVA, p=0.055 in Mann-Whitney U test). This mechanism was not unclear but the data was very important. This data may suggest that suppression of VEGF induced prolongation of effect of endostatin. Next we can try endostatin gene transfection with suppression of VEGF to prove the present data and achieve the tumor dormancy.