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内皮素-1促进CD133^+卵巢肿瘤干细胞血管新生的机制研究 被引量：1

Study on Endothelin-1(ET-1) Contributing to Angiogenesis of CD133^+ Ovarian Cancer Stem Cells
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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.
作者 李青 汪艳 朱慧芬 张曦 胡引男 储芳芳
机构地区 安徽医科大学附属安庆医院
出处 《肿瘤学杂志》 CAS 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)
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) CD133 cancer stem cell angiogenesis hypoxia endothelin-l（ET-1） hypoxia-in-ducible factor lct（I-IIF-lc~） vascular endothelial growth factor（VEGF）
分类号 R73-3 [医药卫生—肿瘤]
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参考文献27

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二级参考文献16

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共引文献4

同被引文献38

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肿瘤学杂志
2013年 第2期

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