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作 者:刘玉海 刘明明 刘新华[2] Liu Yuhai;Liu Mingming;Liu Xinhua(Dept of Emergency and Minimally Invasive Surgery,The Third Affiliated Hospital of Anhui Medical University,Hefei Binhu Hospital,Hefei230022;School of Pharmacy,Anhui Medical University,Hefei230032)
机构地区:[1]安徽医科大学第三附属医院(合肥市滨湖医院)急诊微创外科,合肥230022 [2]安徽医科大学药学院,合肥230032
出 处:《安徽医科大学学报》2019年第11期1672-1677,共6页Acta Universitatis Medicinalis Anhui
基 金:国家自然科学基金(编号:21572003)
摘 要:目的:探讨miR-637对胃癌细胞增殖、凋亡和侵袭的影响及其机制。方法:实时定量PCR(qRT-PCR)检测人胃癌细胞系SCG7901、AGS和正常胃黏膜上皮细胞GES-1中miR-637的表达水平;分别在SCG7901、AGS细胞中转染miR-637 mimics和抑制剂后,用CCK-8检测法、划痕实验、Transwell实验检测miR-637对胃癌细胞增殖、迁移和侵袭能力的影响;qRT-PCR、Western blot法检测miR-637对CDK6及相关蛋白表达的影响。结果:miR-637显著抑制胃癌细胞的增殖、迁移、侵袭能力;过表达miR-637 mimics后CDK6表达下调,而转染miR-637抑制剂后,CDK6表达上调,下游相关蛋白cyclin D、E2F1、p-Rb也有显著变化。结论:miR-637可以抑制胃癌细胞增殖、迁移和侵袭,其机制与靶向CDK6/cyclinD1/Rb信号通路有关。Objective To investigate the effect and mechanism of miR-637 on proliferation,apoptosis and invasion of gastric cancer cells.Methods Real-time quantitative PCR(qRT-PCR)was used to detect the expression levels of miR-637 in human gastric cancer cell line SCG7901,AGS and in gastric epithelial mucosa cell line GES-1.After transfected with miR-637 mimics and inhibitors,cellular proliferation,migration and invasion of SCG7901 and AGS cells was detected by CCK-8,scratch and transwell assays.The expression of CDK6 and related proteins was detected by qRT-PCR and Western blot.Results Transfection of miR-637 mimics significantly inhibited cellular proliferation,migration and invasion while transfection of miR-637 inhibitor was the opposite.Mechanisms studies revealed that miR-637 down-regulated the expression of CDK6,as well as down-stream proteins,such as cyclin D1,E2F1 and the phosphorylation of Rb.Conclusion miR-637 can inhibit cellular proliferation,migration and invasion of gastric cancer with targeting CDK6/cyclinD1/Rb signaling pathway.
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