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目的 探讨miR-124是否能够通过靶向抑制Sp1基因调控入骨肉瘤MG-63细胞的增殖.方法 利用荧光素酶报告基因实验验证Spl基因是否为miR-124的靶基因,应用阳离子脂质体LipofectamineTM2000将miR-124 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Sp1 mRNA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Sp1基因为miR-124的靶基因.与对照组相比,转染miR-124 mimics后,MG-63细胞Sp1 mRNA与蛋白的表达均显著降低,增殖能力明显下降(P＜0.01);与对照组相比,转染miR-124 inhibitor后,MG-63细胞Sp1mRNA与蛋白的表达均显著升高,增殖能力明显升高(P＜0.01).结论 miR-124抑制人骨肉瘤MG-63细胞增殖可能与靶向Sp1基因相关.“,”Objective To investigate whether miR-124 regulates the proliferation of human osteosarcoma cell line MG-63 by targeting Sp1 gene.Methods Luciferase reporter gene assay was used to detect whether Sp1 was target gene of miR-124,miR-124 mimics or inhibitor was transfected into MG-63 cells by lipofectamine package,then realtime PCR and Western blot were used to evaluate the expression of Spl mRNA and protein,respectively,the proliferation of MG-63 cells was analyzed by MTF assay.Results The luciferase reporter gene assay showed that Sp1 was target gene of miR-124;compared with untreated group,the mRNA and protein expression levels of Sp1 and the viability of MG-63 cells were decreased significantly after miR-124 mimics was transfected into MG-63 cells(P＜0.01),but increased significantly after miR-124 inhibitor was transfected into MG-63 cells.Conclusion The inhibition of miR-124 on the proliferation of human osteosarcoma MG-63 cells might be related to targeting Sp1 gene.