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

作　　者：李青[1] 汪艳[1] 朱慧芬[1] 张曦[1] 胡引男[1] 储芳芳[1] 

机构地区：[1]安徽医科大学附属安庆医院,安徽安庆246000

出　　处：《肿瘤学杂志》2013年第2期85-89,共5页Journal of Chinese Oncology

基　　金：安徽省2010年度第四批科技计划项目(10020503083)

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。[Purpose] To investigate the mechanism of angiogCnesis 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-1a 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 hy- poxia 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-lot 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-lc by protease,stabilizes the exoression of HIF-lc,which could stimulate anziozenesis of CD133 cancer stem cells.

关 键 词：CDl33+ 肿瘤干细胞 血管生成 缺氧 内皮素1(ET-1) 缺氧诱导因子la(HIF-1a) 

分 类 号：R73-3[医药卫生—肿瘤]