[1]桂志勇　冯　军　黄俊红　白敬洋.靶向沉默c-fos基因表达对胶质瘤U87MG细胞增殖与侵袭的影响[J].中国临床神经外科杂志,2017,(12):834-838.[doi:10.13798/j.issn.1009-153X.2017.12.011]
　GUI Zhi-yong,FENG Jun,HUANG Jun-hong,et al.Effects of c-fos targeted silence on proliferation and invasiveness of human glioma cell U87[J].,2017,(12):834-838.[doi:10.13798/j.issn.1009-153X.2017.12.011]
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靶向沉默c-fos基因表达对胶质瘤U87MG细胞增殖与侵袭的影响 ()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
期数:
2017年12期
页码:
834-838
栏目:
论著
出版日期:
2017-12-25

文章信息/Info

Title:
Effects of c-fos targeted silence on proliferation and invasiveness of human glioma cell U87
文章编号:
1009-153X（2017）12-0834-05
作者:
桂志勇　冯　军　黄俊红　白敬洋
作者单位：462000 河南，漯河市第一人民医院神经外科（桂志勇、黄俊红）；430022 武汉，华中科技大学同济医学院附属协和医院神经外科（冯　军、白敬洋）
Author(s):
GUI Zhi-yong1;  FENG Jun2;  HUANG Jun-hong1;  BAI Jingyang1.
1. Department of Neurosurgery, the First people's Hospital of Luohe City, Luohe 462000, China; 2. Department of Neurosurgery, Affiliated Union Hospital, Tongji Medical School, Huazhong University of Sciences andTechnology, Wuhan 430022, China
关键词:
胶质母细胞瘤; c-fos; shRNA; 细胞增殖; 细胞侵袭; RNA干扰技术
Keywords:
【Key words】 Human glioma;  c-fos;  shRNA;  Proliferation;  Invasiveness
分类号:
R 739.41; Q 789
DOI:
10.13798/j.issn.1009-153X.2017.12.011
文献标志码:
A
摘要:
目的 探讨靶向沉默c-fos基因表达对胶质瘤U87MG细胞体外增殖与侵袭的影响。方法 构建慢病毒载体c-fos-shRNA，将其转染人脑胶质瘤U87MG细胞，同时将空载体转染细胞作为空载对照，未转染细胞作为空白对照；观察U87MG细胞形态、c-fos mRNA和蛋白表达变化、细胞侵袭和迁移能力、细胞生存率和细胞凋亡率。结果 c-fos-shRNA慢病毒转染U87MG细胞48 h后，荧光显微镜下观察发现空白对照组U87MG细胞无绿色荧光，而空载体组和转染组U87MG细胞可见绿色强荧光和清晰的细胞轮廓。与空白对照组、空载体组相比，转染组U87MG细胞c-fos mRNA和c-fos蛋白表达显著降低（P<0.05）；慢病毒转染U87MG细胞24 h后，转染组U87MG细胞存活率显著降低（P<0.05），细胞活力显著减弱（P<0.05）；细胞迁移和侵袭能力明显减弱（P<0.05）；慢病毒转染72 h后，转染组U87MG细胞凋亡数量显著上升（P<0.05）。结论 沉默c-fos基因表达可显著抑制脑胶质瘤U87MG细胞增殖和侵袭能力。
Abstract:
【Abstract】 Objective To explore the effects of lentivirus-mediated c-fos targeted silence on the proliferation and invasiveness of human glioma cell U87 in vitro. Methods Lentiviral vector c-fos-shRNA was transfected into human glioma U87 cells. Empty vector-transfected human glioma U87 cells served as the no-load control, and non-transfected human glioma U87 cells serve as the blank control. The morphology of U87 cells, the expression of c-fos mRNA and c-fos protein, the invasiveness and migration ability of U87 cells, and the survival rate of glioma cells, and the apoptosis rate of U87 cells were observed in all the groups. Results No green fluorescence of U87 cells in the blank control group, strong green fluorescence and clear cell outline of U87 cells in the no-load group and the transfection group were observed by the fluorescence microscope. The levels of c-fos mRNA and protein expressions were significantly lower in the transfection group 48 hours after the transfection than those in the no-load and blank control groups (P<0.05) The survival rate, migration and invasion ability of U87 cells were significantly lower in the transfection group 48 hours after the transfection than thsoe in the blank control and no-load groups (P<0.05). The number of apoptotic cells was significantly more in transfection group 72 hours after the transfection than that in the blank control and no-load groups (P<0.05). Conclusions It is suggested that c-fos targeted silence can significantly inhibit the proliferation and invasiveness of human glioma U87 cells, and c-fos-shRNA lentivirus-mediated gene therapy may be targeted as a new candidate for c-fos gene therapy.

参考文献/References:

[1] 刘　森，沈　野，于洪飞，等. 基于RNA-seq研究胶质母 细胞瘤中差异表达基因及蛋白相互作用网络[J]. 基因组 学与应用生物学，2017，8（4）：1280-1287. [2] Gudbergsson JM, Elb?k KJ, Stolberg CB, et al. Characteri- zation of glioblastoma multiforme exosomes [J]. Dig Dis Sci, 2015, 43(11): 2398-2404. [3] Amanda S, Varsha H, Zainab A, et al. MicroRNAs in glio- blastoma multiforme pathogenesis and therapeutics [J]. Cancer Med, 2016, 5(8):1917-1946. [4] 董梦梦，孙倩玲，张灵芝，等. CKS2 shRNA慢病毒表达载 体的构建及其抑制卵巢癌A2780细胞增殖[J]. 基础医学 与临床，2016，36（2）：145-150. [5] Yang B, Janardhanan R, Vohra P, et al. Adventitial trans- duction of lentivirus-shRNA-VEGF-A in arteriovenous fistula reduces venous stenosis formation [J]. Kidney Int, 2014, 85(2): 289-306. [6] Chambellan A, Leahy R, Xu W, et al. Pivotal role of c-Fos in nitric oxide synthase 2 expression in airway epithelial cells [J]. Nitric Oxide, 2009, 20(3): 143-149. [7] Liu Z, Yan R, Al-Salman A, et al. Epidermal growth factor induces tumour marker AKR1B10 expression through activator protein-1 signalling in hepatocellular carcinoma cells [J]. Biochem J, 2012, 442(2): 273-282. [8] Senecal A, Munsky B, Proux F, et al. Transcription factors modulate c-Fos transcriptional bursts [J]. Cell Rep, 2014, 8 (1): 75-83. [9] Pozas E, Ballabriga J, Planas AM, et al. Kainic acid- induced excitotoxicity is associated with a complex c-Fos and c-Jun response which does not preclude either cell death or survival [J]. Dev Neurobiol, 2015, 33(3): 232-246. [10] Pan J, Wang H, Liu X, et al. Tumor restrictive suicide gene therapy for glioma controlled by the FOS promoter [J]. PLoS One, 2015, 10(11): e0143112. [11] Figueiredo HF, Bruestle A, Bodie B, et al. The medial pre- frontal cortex differentially regulates stress-induced c-fos expression in the forebrain depending on type of stressor [J]. Eur J Neurosci, 2015, 18(8): 2357-2364. [12] 王　浩，潘建青，胡继良，等. C-fos启动子在人胶质瘤细 胞株及正常组织的转录活性研究[J]. 中华神经医学杂 志，2015，14（7）：669-673. [13] 李　霏，李松林，尹元琴. NK4基因重组慢病毒载体的构 建及在肝癌细胞中的表达[J]. 中国医科大学学报，2011， 40（12）：1081-1084. [14] 史梦婷，孟露萍，包海洋，等. 结核分支杆菌Rv2031c慢病 毒载体的构建及其对RAW264.7细胞凋亡的影响[J]. 动 物医学进展，2015，36（5）：1-5.

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更新日期/Last Update: 2017-12-27