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机构地区:[1]武汉华中科技大学同济医学院附属同济医院骨科,430030
出 处:《肿瘤防治研究》2006年第5期355-357,384,共4页Cancer Research on Prevention and Treatment
摘 要:目的体外研究尿胰蛋白酶抑制剂(urinary trypsininhibitor,UTI)抑制人骨肉瘤细胞系MG-63细胞的侵袭与转移。方法在体外培养的MG-63细胞培养基中加入不同浓度的UTI,对照组中加入50μl PBS缓冲液,用免疫组化、RT-PCR和Western blot方法检测尿激酶型纤溶酶原激活物(urokinasetype plasminogen activator,UPA)的表达情况。结果免疫组化染色、RT-PCR及Western blot检测发现随着UTI浓度的逐渐增加,UPA表达量逐渐减少,当UTI浓度增加到100nM时,抑制作用明显(P<0.05),并且呈剂量依赖性。结论UTI不但从mRNA水平,而且从蛋白质水平抑制骨肉瘤细胞表达UPA,从而抑制骨肉瘤细胞侵袭与转移。Objective In order to investigate the effect of invasion and metastasis of human osteosarcoma MG-63 by the urinary trypsin inhibitor(UTI) in vitro. Methods Different doses (10、50、100、 300、 500nM) of UTI were added into the human osteosarcoma MG-63 medium and 50μl PBS was added into the control at the same time, then the expression of urokinase type plasminogen activator(UPA) was detected by immunohisto-chemistry, RT-PCR and Western blot. Results The more concentration of UTI was transfected,the lesser UPA were expressed by the detections of immunohisto-chemistry and RT-PCR and Western blot. When the concentration became 50nM, the suppression was obvious(P〈0. 05), and the suppression was in dose-dependent manners. Conclusion The UTI can suppress efficiently the expression of protein UPA both at the mRNA level and at the protein level, then suppress the invasion and metastasis in osteosarcoma cells.
关 键 词:尿胰蛋白酶抑制剂 尿激酶型纤溶酶原激活物 骨肉瘤
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