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机构地区:[1]徐州市第一人民医院肿瘤内科,江苏徐州221002 [2]解放军307医院乳癌内科,北京100071
出 处:《肿瘤基础与临床》2009年第1期27-29,共3页journal of basic and clinical oncology
摘 要:目的探讨不同浓度表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对人甲状腺乳头状癌细胞(K1)凋亡的诱导作用及对其Survivin蛋白表达的影响。方法4种不同浓度的EGCG(20、40、80、160μg/mL)处理甲状腺乳头状癌细胞株K124h、48h,MTT法测定EGCG对K1细胞增殖活性的影响;流式细胞仪检测48h后各浓度EGCG诱导K1细胞凋亡的作用;免疫组化S-P法检测Survivin蛋白在K1细胞中的表达及各浓度EGCG作用48h后Survivin蛋白表达的变化。结果EGCG显著抑制K1细胞的增殖,其抑制作用呈时间、剂量依赖性(P<0.01)。EGCG诱导K1细胞凋亡,凋亡率随EGCG浓度的增加而增加(P<0.01)。Survivin蛋白在K1细胞中高表达,EGCG抑制Survivin蛋白的表达,其表达水平随EGCG浓度的增加而减少(P<0.01)。结论EGCG抑制K1细胞中Survivin蛋白的表达,这可能是EGCG抑制K1细胞增殖、诱导其凋亡的主要机制。Objective To investigate the apoptosis in thyroid papillary carcinoma cells(K1) induced by different concentrations of epigallocatechin-3-gallate (EGCG) and to study EGCG' s influence on the expressions of Survivin protein. Methods Cell proliferation was examined by MTT assay at two different time points ; the apoptosis of K1 cells was tested by flow cytometry ; the expressions of survivin protein were analyzed by immuno-histochemical method in EGCG-treated and untreated K1 cells. Results EGCG inhibited the proliferation of K1 cells, this function depended upon EGCG-treated time and EGCG' s concentration. The apoptosis of K1 cells was induced by EGCG, apoptotic rate was increased step by step when EGCG' s concentration was raised. In EGCG non-used K1 cells, the expressional level of Survivin protein was significantly high ; and it was obvious that the expressions of Survivin protein were effectively inhibited after EGCG was used. Conclusion EGCG can inhibit the growth of K1 cells and induce cell apoptosis,its mechanism may be principally associated with blocking Survivin expressions.
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