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机构地区:[1]华中科技大学同济医学院附属协和医院肿瘤中心,武汉430023
出 处:《肿瘤》2009年第1期49-52,共4页Tumor
摘 要:目的:研究血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)及血管紧张素Ⅱ1型受体(angiotensinⅡ type 1 receptor,AT1R)阻滞剂缬沙坦对鼻咽癌细胞株CNE-2血管内皮生长因子(vascular endothelial growth factor,VEGF)表达及其生物学行为的影响。方法:应用RT-PCR和ELISA法分别检测干预前后CNE-2细胞VEGF基因和蛋白水平表达的变化。采用MTT法检测AngⅡ对CNE-2细胞增殖的影响。采用体外侵袭实验检测AngⅡ和缬沙坦对CNE-2细胞侵袭力的影响。结果:AngⅡ可诱导CNE-2细胞表达VEGF(P<0.05),并呈剂量依赖效应。AngⅡ可提高CNE-2细胞增殖率和侵袭能力(P<0.05),而缬沙坦可抑制AngⅡ的诱导作用。结论:AngⅡ可诱导鼻咽癌CNE-2细胞的增殖和侵袭,AT1R阻滞剂可抑制此种诱导作用,其机制可能涉及对VEGF的表达调控。Objective: To investigate the effects of angiotensin Ⅱ (Ang Ⅱ ) and Aug U type 1 receptor (AT1 R) blocker valsartan on vascular endothelial growth factor (VEGF) expression and biological behavior of nasopharyngeal carcinoma cells. Methods: VEGF expression and secretion in CNE-2 cells were determined by RT-PCR and ELISA, respectively, in vitro. Effects of Ang Ⅱ and AT1R blocker on the proliferation of nasopharyngeal carcinoma cells were evaluated by MTT assay in vitro and the influence of Ang Ⅱ and valsartan on the invasion capacity of cells CNE-2 was detected by 24-well Matrigel invasion test. Results: Ang Ⅱ dose-dependently induced the expression and secretion of VEGF in nasopharyngeal carcinoma cells in vitro and enhanced the proliferation and invasion capacity of CNE-2 cells ( Both P 〈 0.05 ). AT1R blocker valsartan reversed the effect of Ang Ⅱ. Conclusion: Ang Ⅱ induced proliferation and invasion of nasopharyngeal carcinoma cell while AT1R blocker valsartan inhibited it. The underlying mechanism may be related with regulation of VEGF expression and secretion.
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