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机构地区:[1]重庆医科大学附属第一医院神经外科,重庆400016
出 处:《第三军医大学学报》2008年第2期157-160,共4页Journal of Third Military Medical University
摘 要:目的研究LRIG1诱导神经胶质瘤细胞的凋亡作用,探讨LRIG1对表皮生长因子受体信号转导通路抑制效应的分子机制。方法采用Lipofectamine介导的基因转染技术,将质粒pcDNA3.1-LRIG1转染原代神经胶质瘤细胞,应用逆转录聚合酶链反应(RT-PCR)和Western blot方法检测转染后胶质瘤细胞LRIG1和EGFR mRNA与蛋白水平的变化,Western blot方法检测神经胶质瘤细胞PKCα、Bax、bcl-2蛋白水平的变化。MTT法和流式细胞技术分析细胞的增殖和凋亡的变化。结果细胞中转染pcDNA3.1-LRIG1组中以LRIG1 mRNA和蛋白质的表达水平较未处理组和转染空载体组明显升高,而EGFR mRNA和蛋白质的表达水平较对照组和转染空载体组明显降低,PKCα、Bax表达上调,bc1-2表达下降,胶质瘤细胞生长受到抑制,凋亡显著增强。结论LRIG1可能通过参与形成EGFR的负反馈环,从多种途径抑制了肿瘤的生长。Objective To explore the molecular mechanism that LRIG1 inhibits signal transduction system of epidermal growth factor receptor (EGFR) by investigating the role of LRIG1 in glioma. Methods The plasmid pcDNA3.1-LRIG1 was transfected into primary glioma cells by Lipofectamine. Then, the changes of LRJG1 and EGFR in the transfected glioma cells were measured by RT-PCR and Western blot, and the cell proliferation and apoptosis were analyzed by MTY and flow cytometry. Results The expression levels of LRIG1 mRNA and protein in the glioma cells transfected with pcDNA-LRIG1 were significantly higher than those of control group and pcDNA3, 1 transfected glioma cells, while those of EGFR mRNA and protein were significantly lower. The expression of PKCα and Bax was up-regulated, while the expression of bcl-2 was down-regnlated, The growth of glioma cells was inhibited and their apoptosis was obviously enhanced. Conclusion By participating the construction of the negative feedback loop of EGFR, LRIG1 inhibits the occurrence and growth of tumor through several pathways.
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