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Survivin specific siRNA associated with paclitaxel synergistically inhibits glioma U-87MG cells proliferation and related mechanism

机译:与紫杉醇相关的Survivin特异性siRNA协同抑制胶质瘤U-87mg细胞增殖和相关机制

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In order to explore the effect of paclitaxel (PTX) combined with Survivin siRNA on proliferation and apoptosis in U-87MG cells in vitro, the U-87MG cells were transfected with Survivin siRNA and treated with PTX at the same time. The cell morphological changes were determined by methylene blue solution. Survivin, cyclin D1, c-Myc and CDK4 expression in U-87MG cells was analyzed by RT-PCR and western blot at 48 h after treatment. The cell proliferation and apoptosis in U-87MG cells were determined by MTT, flow cytometry assay. The results showed that Survivin was highly expressed in U-87MG cells, whereas Survivin expression was reduced in pSilenceTMneo3.1 — H1-siRNA — Survivin transfected and PTX treated U-87MG cells separately. But the inhibiting effect is not so obvious, in order to improve the treatment effect, PTX and survivin siRNA were used to treat U-87MG cells at the same time. The results demonstrated that Survivin siRNA combined with PTX significantly increased the sensitivity of U-87MG cells of PTX and elevated apoptotic cell rate, thus decreased, CDK4, cyclin D1 and c-Myc expression levels in U-87MG cells through RT-PCR and western blot assays. In short, this study demonstrated that Survivin siRNA combined PTX effectively suppressed growth and induced apoptosis in U-87MG cells in vitro, it is an vital approach to treat glioma.
机译:为了探讨紫杉醇(PTX)与Survivin siRNA在体外对U-87MG细胞中的增殖和凋亡的影响,用Survivin siRNA转染U-87mg细胞并同时用PTX处理。细胞形态变化由亚甲基蓝溶液测定。通过RT-PCR和治疗后48小时分析U-87mg细胞中的Survivin,Cyclin D1,C-Myc和CDK4表达。通过MTT,流式细胞术测定测定U-87mg细胞中细胞增殖和凋亡。结果表明,Survivin在U-87mg细胞中高度表达,而Survivin表达在psilencetmneo3.1 - h1-siRNA - survivin转染和Ptx处理的U-87mg细胞中。但抑制效果并不是明显的,为了改善治疗效果,PTX和Survivin siRNA用于同时治疗U-87mg细胞。结果表明,Survivin siRNA与PTX结合显着增加了PTX的U-87mg细胞的敏感性,并通过RT-PCR和Western降低了U-87Mg细胞中的CDK4,Cyclin D1和C-Myc表达水平印迹测定。简而言之,本研究表明,Survivin siRNA组合PTX在体外有效地抑制了U-87MG细胞中的生长和诱导细胞凋亡,这是治疗胶质瘤的重要方法。

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