RNA干扰核因子IA对胶质瘤细胞侵袭迁移能力的实验研究
发布时间：2018-12-17 19:01
【摘要】：目的 本研究旨在探究核因子IA(nuclear factor IA,NFIA)在胶质瘤发生发展中的作用机制,并观察NFIA和ezrin在胶质瘤中表达相关性,并进一步探讨NFIA促进胶质瘤细胞侵袭转移的分子机制。方法使用siRNA干扰技术处理胶质瘤U251细胞,采用实时荧光定量PCR(realtime-PCR)和Western blot检测NFIA表达水平的变化,采用划痕实验及transwell小室侵袭实验检测敲低NFIA蛋白表达对胶质瘤细胞侵袭、迁移能力的变化。结果 下调胶质瘤细胞株中NFIA后,NFIA干扰组细胞生长明显减慢,与阴性对照组与空白对照组比较,差异均有统计学意义(P0.05)。划痕实验显示NFIA干扰组细胞迁移距离(57.9±6.9)μm明显低于阴性对照组(125.4±10.7)μm和空白对照组(111.5±5.9)μm,差异有统计学意义(P0.05),Transwell实验显示RNA干扰组穿膜细胞数(33.3±3.2)低于阴性对照组和空白对照组(80.3±4.5、87.7±5.0),差异有统计学意义(P0.05)。Western blot结果显示,NFIA干扰组Ezrin的蛋白相对表达显著低于阴性对照组与空白对照组,差异均有统计学意义(P0.05)。讨论 在胶质瘤组织中NFIA表达明显高于正常脑组织,下调NFIA蛋白表达可抑制胶质瘤细胞侵袭和迁移能力。
[Abstract]:Objective to investigate the role of nuclear factor IA (nuclear factor IA,NFIA in the pathogenesis of glioma, and to investigate the correlation between NFIA and ezrin expression in gliomas, and to explore the molecular mechanism of NFIA promoting the invasion and metastasis of glioma cells. Methods siRNA interference technique was used to treat U251 glioma cells and real-time quantitative PCR (realtime-PCR) and Western blot were used to detect the expression of NFIA. Scratch test and transwell chamber invasion assay were used to detect the changes of the invasion and migration ability of glioma cells induced by low expression of NFIA protein. Results after down-regulation of NFIA in glioma cell line, the cell growth of NFIA interference group was significantly slower than that of negative control group and blank control group (P0.05). The cell migration distance of NFIA interference group (57.9 卤6.9) 渭 m was significantly lower than that of negative control group (125.4 卤10.7) 渭 m and blank control group (111.5 卤5.9) 渭 m (P0.05). Transwell test showed that the number of perforating cells in RNA interference group (33.3 卤3.2) was significantly lower than that in negative control group and blank control group (80.3 卤4.5 卤87.7 卤5.0), and the difference was statistically significant (P0.05). Western blot). The relative expression of Ezrin protein in NFIA interference group was significantly lower than that in negative control group and blank control group (P0.05). The expression of NFIA in glioma tissue was significantly higher than that in normal brain tissue, and down-regulation of NFIA protein expression could inhibit the invasion and migration of glioma cells.
【学位授予单位】：皖南医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R739.41
本文编号：2384663
[Abstract]:Objective to investigate the role of nuclear factor IA (nuclear factor IA,NFIA in the pathogenesis of glioma, and to investigate the correlation between NFIA and ezrin expression in gliomas, and to explore the molecular mechanism of NFIA promoting the invasion and metastasis of glioma cells. Methods siRNA interference technique was used to treat U251 glioma cells and real-time quantitative PCR (realtime-PCR) and Western blot were used to detect the expression of NFIA. Scratch test and transwell chamber invasion assay were used to detect the changes of the invasion and migration ability of glioma cells induced by low expression of NFIA protein. Results after down-regulation of NFIA in glioma cell line, the cell growth of NFIA interference group was significantly slower than that of negative control group and blank control group (P0.05). The cell migration distance of NFIA interference group (57.9 卤6.9) 渭 m was significantly lower than that of negative control group (125.4 卤10.7) 渭 m and blank control group (111.5 卤5.9) 渭 m (P0.05). Transwell test showed that the number of perforating cells in RNA interference group (33.3 卤3.2) was significantly lower than that in negative control group and blank control group (80.3 卤4.5 卤87.7 卤5.0), and the difference was statistically significant (P0.05). Western blot). The relative expression of Ezrin protein in NFIA interference group was significantly lower than that in negative control group and blank control group (P0.05). The expression of NFIA in glioma tissue was significantly higher than that in normal brain tissue, and down-regulation of NFIA protein expression could inhibit the invasion and migration of glioma cells.
【学位授予单位】：皖南医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R739.41
【参考文献】
相关期刊论文 前3条
1 王爽;李仕晟;谢鼎华;唐青来;王树辉;刘家佳;陈月红;杨新明;;CD44调控鼻咽癌上皮-间质转化及转移的实验研究[J];临床耳鼻咽喉头颈外科杂志;2013年05期
2 高书颖;李恩民;孟令英;崔磊;袁华敏;杜则澎;许丽艳;;肺癌细胞中调控ezrin基因基本转录活性的顺式作用元件及转录因子的鉴定[J];生物化学与生物物理进展;2009年03期
3 孙琦蛮,樊嘉,刘银坤,周俭,余耀,邱双健,吴志全;Ezrin在肝癌中的表达及其与肿瘤黏附、侵袭和门静脉癌栓的关系[J];复旦学报(医学版);2005年02期
，本文编号：2384663
本文链接：https://www.wllwen.com/yixuelunwen/zlx/2384663.html
