塞来昔布对人骨肉瘤MG-63细胞增殖、凋亡及PI3K/Akt信号通路的影响
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  • 英文篇名:Effect of Celecoxib on the Proliferation and Apoptosis of MG-63 Cells Through PI3K/Akt Pathway
  • 作者:段大鹏 ; 秦静 ; 祁洁 ; 刘军 ; 李全义 ; 弓立群
  • 英文作者:DUAN Dapeng;QIN Jing;QI Jie;Shaanxi Provincial People's Hospital;
  • 关键词:塞来昔布 ; 骨肉瘤 ; PI3K/Akt信号通路 ; 增殖 ; 凋亡
  • 英文关键词:Celecoxib;;Osteosarcoma;;PI3K/Akt pathway;;Proliferation;;Apoptosis
  • 中文刊名:SYAZ
  • 英文刊名:The Practical Journal of Cancer
  • 机构:陕西省人民医院;
  • 出版日期:2019-02-25
  • 出版单位:实用癌症杂志
  • 年:2019
  • 期:v.34;No.203
  • 基金:陕西省自然科学基础研究项目(编号:2016JQ8052);; 陕西省中医管理局中医药科研课题(编号:JCMS048)
  • 语种:中文;
  • 页:SYAZ201902001
  • 页数:3
  • CN:02
  • ISSN:36-1101/R
  • 分类号:5-7
摘要
目的观察COX-2选择性抑制剂塞来昔布对人骨肉瘤细胞株MG-63的增殖、凋亡及PI3K/Akt信号通路的影响。方法对数生长期人骨肉瘤细胞株MG-63细胞用不同浓度的塞来昔布溶液(0、25、50和100μmol/L)处理后,MTT比色法检测24 h、48 h及72 h各组细胞增殖活性的影响;流式细胞仪测定各组细胞凋亡率; Western blot检测COX-2、CAS-3和P-Akt蛋白表达变化。结果塞来昔布对MG-63细胞具有抑制增殖的作用,且该作用与药物浓度及作用时间呈正相关;流式细胞术检测结果显示细胞凋亡率与塞来昔布浓度呈正相关;随着塞来昔布浓度的增加,COX-2和P-Akt蛋白的表达水平逐渐降低,而CAS-3表达水平逐渐升高。结论塞来昔布抑制MG-63细胞增殖,促使细胞凋亡,其机制与下调PI3K/Akt信号通路有关。
        Objective To explore the effect of Celecoxib on the proliferation and apoptosis of MG-63 cells,and elucidated the correlation between the effect and PI3 K/Akt pathway. Methods Cultured MG-63 cells were treated with different concentration of Celecoxib( 0,25,50 and 100 μmol/L),MTT assay was used to test the cell proliferation,and the rates of apoptosis of cells were assessed by the flow cytometry. Western blot were emplored to examine the expression of COX-2,CAS-3 and P-Akt in cultured MG-63 cells. Results Celecoxib could inhibit the proliferation of MG-63 cells significantly in a dose and time dependent manner,and compared to control,the apoptosis rate significantly increased with increases in concentrations of celecoxib; Furthermore,The level of COX-2,CAS-3 and P-Akt protein expression were significantly down-regulated with increases in concentrations of celecoxib( P < 0. 05). Conclusion The inhibition of proliferation and apoptosis in MG-63 cells could be induced significantly,and its mechanism might be the down regulation of the expression of PI3 K/Akt pathway.
引文
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