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[目的]研究内皮素-1(ET-1)促进CD133+肿瘤干细胞血管新生的机制。[方法]ET-1作用CD133+肿瘤干细胞48h后,通过ELISA法检测细胞内血管内皮生长因子(VEGF)表达量;Northern blot检测VEGF mRNA表达量;Western blot检测缺氧诱导因子-1α(HIF-1α)含量。[结果]在正常条件和缺氧条件下,经ET-1处理的细胞VEGF表达明显高于对照组(P<0.05);BQ123+ET-1组细胞内VEGF mRNA量明显低于ET-1组(P<0.05);经ET-1处理后,细胞从缺氧转到正常条件下,细胞内HIF-1α稳定性增强。[结论]ET-1通过其受体A(ETAR)介导CD133+细胞的VEGF表达上调;降低HIF-1α被蛋白酶降解速度,稳定HIF-1α的表达,从而促进CD133+肿瘤干细胞血管新生。
[Objective] To investigate the mechanism of endothelin-1 (ET-1) promoting angiogenesis in CD133 + tumor stem cells. [Methods] After treated with ET-1 for CD133 + tumor stem cells for 48h, the expression of vascular endothelial growth factor (VEGF) was detected by ELISA. The expression of VEGF mRNA was detected by Northern blot. The expression of HIF-1α )content. [Results] Under normal conditions and hypoxia, the expression of VEGF in ET-1-treated cells was significantly higher than that in control group (P <0.05). The amount of VEGF mRNA in BQ123 + ET-1 group was significantly lower than that in ET-1 group (P <0.05). The stability of HIF-1α in cells after ET-1 treatment increased from hypoxia to normal condition. [Conclusion] ET-1 can up-regulate the expression of VEGF in CD133 + cells through its receptor A (ETAR), decrease the degradation rate of HIF-1α by proteases, and stabilize the expression of HIF-1α, thereby promoting the angiogenesis of CD133 + tumor stem cells.