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作 者:贾雪峰[1] 陈文明[1] 孙道萍[1] 赵海波[1] 蒋树龙[1] 刘宁[1] 阳帆[2]
机构地区:[1]山东省济宁市第一人民医院肿瘤科,山东济宁272111 [2]湘南学院基础医学部,湖南郴州423000
出 处:《海南医学院学报》2015年第8期1030-1032,共3页Journal of Hainan Medical University
基 金:湖南省教育厅计划项目(13C91)~~
摘 要:目的:研究槲皮素对TGFβ-1诱导的人胃癌BGC-803细胞上皮间质转化的影响及机制。方法:将胃癌BGC-803细胞分为3组,分别为正常对照组、TGFβ-1组、TGFβ-1+槲皮素组,分别在第12、24、48和72h后,采用MTT法检测各组细胞增殖能力,划痕修复实验检测各组细胞迁移能力;并采用Western blot实验检测上皮间质转化因子,E-cadherin、N-cadherin和Vimentin的表达情况。同时对PI3K/AKT信号转导通路的活性进行评价。结果:与TGFβ-1组相比,槲皮素降低了人胃癌BGC-803细胞的增值能力、迁移能力;TGFβ-1+槲皮素组E-cadherin表达水平上调,N-cadherin、Vimentin的表达下调。TGFβ-1+槲皮素组的AKT、p-AKT表达水平下调,PI3K/AKT信号转导通路活性降低。结论:槲皮素能够抑制TGFΒ-1诱导的胃癌细胞系的EMT过程,其发生机制可能与调控PI3K/AKT信号转导通路活性有关。Objective:To explore the effects of quercetin on the epithelial-mesenchymal transition of human gastric carcinoma BGC-803 cells induced by TGFβ-1and its mechanism.Methods:Gastric carcinoma BGC-803 cells were divided into three groups,i.e.normal control group,TGFβ-1,and TGFβ-1+quercetin group.After 12,24,48,and 72 h,MTT was used to detect the cell proliferation capability,scratch repair experiment was used to detect the cell migration ability,and Western blot was utilized for determining the expressions of epithelial-mesenchymal transition factor,E-cadherin,N-cadherin and Vimentin.Meanwhile,the activity of PI3K/AKT signal transduction pathway was evaluated.Results:Compared with the TGFβ-1group,quercetin reduced the proliferation capability and migration ability of human gastric carcinoma BGC-803 cells.In the TGFβ-1+quercetin group,E-cadherin expression level was up-regulated,N-cadherin,Vimentin,AKT,and p-AKT expression levels were down-regulated,and the activity of PI3K/AKT signal transduction pathway was reduced.Conclusions:Quercetin can inhibit the EMT process of human gastric cancer cell lines induced by TGFβ-1.The pathogenetic mechanism is probably associated with the regulation of PI3K/AKT signal transduction pathway activity.
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