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机构地区:[1]广州医科大学附属第二医院神经外科,广州510260
出 处:《国际神经病学神经外科学杂志》2016年第6期521-525,共5页Journal of International Neurology and Neurosurgery
摘 要:目的探讨长链非编码RNA(Long noncoding RNAs,LncRNAs)H19在人多形性胶质母细胞瘤((glioblastoma mutliforme,GBM)中的表达及其对U87-GBM生物学功能的影响及作用机理。方法实时荧光定量核酸扩增检测系统(Realtime Quantitative PCR Detecting System,qPCR)检测H19在GBM表达;CCK-8试剂盒(Cell Counting Kit-8,CCK-8)检测U87细胞增殖;流式细胞技术(Flow Cytometry,FCM)检测U87细胞凋亡及细胞周期;侵袭小室(transwell)检测U87细胞迁移和侵袭.蛋白质印迹法(Western blot)法检测P53表达。结果 H19在GBM中高表达,上调H19促进GBM的增殖、侵袭、迁移;抑制凋亡;增加了细胞周期S期比例;抑制了P53的表达。结论 H19促进GBM的致癌性。Objective To investigate the expression of H19 (a long noncoding RNA) in human glioblastoma multiforme (GBM), its effect on the biological function of U87-GBM, and the mechanism. Methods The expression of H19 in GBM was determined by the real-time quantitative PCR detection system. The Cell Counting Kit-8 was used to determine the proliferation of U87 cells. Flow cytom- etry was used to assess the apoptosis and cell cycle of U87 cells. The migration and invasion of U87 cells were detected by transwell as- say. Western blot was used to measure the expression of p53. Results H19 was highly expressed in GBM. The overexpression of H19 promoted the proliferation, invasion, and migration of GBM and inhibited the apoptosis of GBM. In addition, the overexpression of H19 increased the proportion of ceils in S phase and inhibited the expression of p53. Conclusions H19 can promote the carcinogenesis of GBM.
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