李 青,汪 艳,朱慧芬.内皮素-1促进CD133+卵巢肿瘤干细胞血管新生的机制研究[J].肿瘤学杂志,2013,19(2):85-89.
内皮素-1促进CD133+卵巢肿瘤干细胞血管新生的机制研究
Study on Endothelin-1(ET-1) Contributing to Angiogenesis of CD133+ Ovarian Cancer Stem Cells
投稿时间:2012-12-16  
DOI:10.11735/j.issn.1671-170X.2013.02.B2012504
中文关键词:  CD133+  肿瘤干细胞  血管生成  缺氧  内皮素1(ET-1)  缺氧诱导因子1α(HIF-1α)  血管内皮生长因子(VEGF)
英文关键词:CD133+  cancer stem cell  angiogenesis  hypoxia  endothelin-1(ET-1)  hypoxia-inducible factor 1α(HIF-1α)  vascular endothelial growth factor(VEGF)
基金项目:安徽省2010年度第四批科技计划项目(10020503083)
作者单位
李 青 安徽医科大学附属安庆医院 
汪 艳 安徽医科大学附属安庆医院 
朱慧芬 安徽医科大学附属安庆医院 
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中文摘要:
      摘 要:[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。
英文摘要:
      Abstract:[Purpose] To investigate the mechanism of angiogenesis of CD133+ cancer stem cells promoted by endothelin-1(ET-1).[Methods] After CD133+ cancer stem cells was treated by ET-1 for 48h,VEGF and HIF-1α were detected by ELISA and Western blot respectively. Northern blot was explored to evaluate the expression of VEGF mRNA. [Results] The expression of VEGF in cells treated with ET-1 was obviously higher than that of the control group under normal and hypoxia condition(P<0.05). But the expression of VEGF mRNA of cells treated with BQ123 and ET-1 was reduced compared to cells treated with ET-1(P<0.05). After treatment with ET-1,HIF-1α was stabilized. [Conclusion] ET-1 contributes to the expression of VEGF in CD 133+ cancer stem cells via ETAR receptor. It also slows down degradation velocity of HIF-1α by protease,stabilizes the expression of HIF-1α,which could stimulate angiogenesis of CD133+ cancer stem cells.
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