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目的探讨肿瘤坏死因子受体相关因子4(TRAF4)对人脑胶质瘤细胞U87增殖、迁移和侵袭的影响。方法运用小干扰技术RNA(siRNA)转染人脑胶质瘤U87细胞,分成阴性对照组(A组)和TRAF4-siRNA组(B组)。检测TRAF4蛋白、MMP-2、MMP-9、p-Akt和周期蛋白D1。应用CCK-8细胞增殖实验检测U87细胞的增殖能力。细胞划痕实验及Transwell迁移、侵袭实验检测U87细胞的迁移、侵袭能力。结果与A组比较,B组U87细胞中TARF4蛋白表达量降低,MMP-2、MMP-9、p-Akt和周期蛋白D1表达量均减少(P<0.05),B组U87细胞增殖能力较低,细胞划痕宽度增大(P<0.05)。Transwell迁移和侵袭实验显示,B组穿过底层膜细胞数均少于A组[(167±5)个vs.(331±8)个和(155±5)个vs.(347±7)个](P<0.05)。结论TRAF4-siRNA靶向干扰了TRAF4的表达,同时下调MMP-2、MMP-9、p-Akt和周期蛋白D1的表达。TRAF4表达下调能降低人脑胶质瘤细胞U87增殖、迁移和侵袭的能力。
Objective To investigate the effect of tumor necrosis factor receptor associated factor 4 (TRAF4) on the proliferation, migration and invasion of human glioma U87 cells. Methods Human glioma U87 cells were transfected with small interfering RNA (siRNA) and divided into negative control group (group A) and TRAF4-siRNA group (group B). TRAF4 protein, MMP-2, MMP-9, p-Akt, and cyclin D1 were detected. Application of CCK-8 cell proliferation assay U87 cell proliferation. Cell scratch assay and Transwell migration, invasion assay U87 cell migration and invasion. Results Compared with group A, the expression of TARF4 protein, the expression of MMP-2, MMP-9, p-Akt and cyclin Dl in U87 cells of group B were decreased (P <0.05), and the proliferation of U87 cells in group B was lower , Cell scratch width increased (P <0.05). Transwell migration and invasion assays showed that the number of cells across the bottom membrane in group B was significantly less than those in group A [(167 ± 5) vs. (331 ± 8) and (155 ± 5) vs. (347 ± 7) ] (P <0.05). Conclusion TRAF4-siRNA targeting interferes with TRAF4 expression and down-regulates MMP-2, MMP-9, p-Akt and cyclin D1 expression. Down-regulation of TRAF4 can reduce the proliferation, migration and invasion of human glioma U87 cells.