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目的证明间质作用因子(stromal interaction molecule1,Stim1)在FBJ诱导的小鼠骨肉瘤细胞中的抑癌作用。方法在Stim1高表达的FBJ-S1-H细胞采用Stim1以siRNA干扰技术得到Stim1沉默的几株S1-H单克隆细胞株,通过细胞行为学方法和RT-PCR技术对其mRNA进行研究,通过明胶酶谱法对细胞基质金属酶活性进行研究。结果通过细胞行为学方法证明,Stim1的沉默提高了细胞的迁移性,通过对mRNA表达的研究发现,Stim1沉默引起了多种基因表达的变化,其中包括基质金属酶9(matrix mexalloprotelnase 9,MMP-9)的升高,窖蛋白(caveolinl,Cav1),甾醇调控因子Srebf1的降低等,提高单克隆细胞中的Cav1含量可以使细胞迁移性降低。结论实验结果证明在FBJ-S1-H细胞中,Stim1能够抑制细胞的移动性,沉默Stim1的表达能够提高细胞的迁移性。
Objective To demonstrate the antitumor effect of stromal interaction molecule1 (Stim1) in FBJ-induced murine osteosarcoma cells. Methods Several S1-H monoclonal cell lines with Stim1 silencing were obtained by Stim1 siRNA targeting Stim1-overexpressing FBJ-S1-H cells. Their mRNAs were studied by cell behavior assay and RT-PCR. Zymography of cell matrix metalloenzyme activity. The results showed that Stim1 silencing increased the cell migration by cell behavior. Stim1 silencing caused a variety of gene expression changes, including matrix mexalloporotelnase 9 (MMP- 9), caveolin1 (Cav1) and steroid regulator Srebf1, etc. The increase of Cav1 content in monoclonal cells can reduce the cell migration. Conclusion The results of experiments show that Stim1 can inhibit cell motility in FBJ-S1-H cells and silencing Stim1 can increase cell migration.