【摘要】 目的探讨miR-21是否能够通过靶向抑制FasL基因调控人骨肉瘤MG-63细胞的增殖。方法利用荧光素酶报告基因实验验证FasL基因是否为miR-21的靶基因,应用阳离子脂质体Lipofectamine^TM2000将miR-21 mimics或inhibitor转染至MG-63细胞,利用real-time PCR和Western blotting分析转染后MG-63细胞FasL m RNA和蛋白表达的变化,通过MTT法分析转染后MG-63细胞增殖水平变化。结果荧光素酶报告基因实验证实FasL基因为miR-21的靶基因。与对照组相比,转染miR-21 mimics后,MG-63细胞FasL mRNA与蛋白的表达均显著降低,增殖能力明显升高（P<0.01）;与对照组相比,转染miR-21 inhibitor后,MG-63细胞FasL mRNA与蛋白的表达均显著升高,增殖能力明显降低,P<0.01。结论 miR-21可能通过靶向FasL基因促进人骨肉瘤MG-63细胞增殖。更多还原

【Abstract】 Objective To investigate whether miR-21 could regulate the proliferation of human osteosarcoma cell line MG-63 by targeting FasL gene.Methods Luciferase reporter gene assay was used to detect whether FasL was target gene of miR-21. miR-21 mimics or inhibitor were transfected into MG-63 cells by lipofectamine package, then real-time PCR and western blot were used to evaluate the expression of FasL mRNA and protein, respectively, the proliferation of MG-63 cells was analyzed by MTT assay.Results The luciferase reporter gene assay showed that FasL was target gene of miR-21. Compared with untreated group, the m RNA and protein expressions of FasL were decreased significantly after miR-21 mimics was transfected into MG-63 cells, but the viability of MG-63 cells was increased significantly(P<0.01). Compared with untreated group, the m RNA and protein expression levels of FasL were increased significantly after miR-21 inhibitor was transfected into MG-63 cells, but the viability of MG-63 cells was decreased significantly( P<0.01). Conclusion The promotion of miR-21 on the proliferation of human osteosarcoma MG-63 cells might be related to targeting FasL gene.更多还原