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作 者:臧晋[1] 王一维[1] 王欣[1] 王正东[1] 王效杰[1]
机构地区:[1]沈阳医学院人体解剖学教研室,辽宁沈阳110034
出 处:《临床军医杂志》2016年第9期900-903,共4页Clinical Journal of Medical Officers
基 金:沈阳市科技局科学计划项目(F13-221-9-33)
摘 要:目的探讨过表达迁移侵袭抑制蛋白(MIIP)基因对人胶质母细胞瘤细胞系U87放疗敏感性的影响。方法采用过表达MIIP基因慢病毒转染U87细胞,通过Western blot实验检测转染效率;MTT实验检测MIIP基因对U87细胞活力的影响;应用平板克隆形成实验,评价放射线照射对MIIP过表达组与对照组克隆形成能力的影响;进一步应用Western blot实验检测RAD51蛋白与BCL2蛋白的表达情况。结果 MIIP基因过表达可以抑制神经胶质瘤细胞U87的增殖能力。上调MIIP基因,抑制U87细胞的克隆形成能力,并提高放疗敏感性。放疗前与放疗后,MIIP基因均抑制RAD51蛋白与BCL2蛋白的表达。结论过表达MIIP基因抑制U87细胞的增殖能力与克隆形成能力;MIIP基因可提高U87细胞放疗敏感性,其机制与RAD51、BCL2信号转导通路相关。Objective To explore the effect of overexpression of migration and invasion inhibitory protein( MIIP) on the radiosensitivity of human glioblastoma cell line U87. Methods MIIP overexpression in cell line U87,and lentivirus transfection efficiency was detected by Wetern blot. The effect of MIIP on the proliferation of U87 cells was assessed through MTT assay. The irradiation sensitivity of MIIP in U87 group and the control group were evaluated by plate clone formation assay. Wetern blot assay was further used to detect the expression of RAD51 protein and BCL2 protein. Results Overexpression of MIIP could inhibit the proliferation of glioblastoma cell U87. Up-regulation of MIIP expression could inhibit the ability of U87 cells to clone and improved the sensitivity of radiotherapy.The expression of RAD51 protein and BCL2 protein could be inhibited by MIIP before and after radiotherapy. Conclusion MIIP inhibits the proliferation and clonal formation of U87 cells,which can enhance the radiosensitivity of U87 cells and its mechanism is related to RAD51 and BCL2 signaling pathway.
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