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目的探讨miR-193a-3p对人Hep-2喉癌细胞增殖、凋亡、侵袭的影响及相关机制。方法用脂质体2000将miR-193a-3p成熟体模拟物(A组)及相应的阴性对照片段(B组)转染Hep-2细胞,以未转染组(C组)作空白对照。MTT法测定各组细胞的增殖能力,流式细胞术检测各组细胞的凋亡情况,Transwell侵袭实验检测各组细胞的侵袭能力,实时定量PCR法检测各组miR-193a-3p的表达,Western blot检测抗凋亡因子髓细胞白血病基因(Mcl-1)蛋白的表达。结果与B、C组相比,转染48h后,A组细胞增殖率降低(P<0.05),细胞凋亡率升高(P<0.05),穿过聚碳酸酯膜的细胞数减少(P<0.01),miR-193a-3p表达水平升高(P<0.05),Mcl-1蛋白表达水平降低(P<0.05)。结论 miR-193a-3p可能通过调控Hep-2细胞中Mcl-1基因的表达,抑制细胞的增殖、侵袭能力,促进其凋亡。
Objective To investigate the effect of miR-193a-3p on proliferation, apoptosis and invasion of human Hep-2 laryngeal carcinoma cells and its related mechanism. Methods Hep-2 cells were transfected with miR-193a-3p mature simulant (group A) and corresponding negative control group (group B) by lipofectamine 2000. The untransfected group (group C) was used as a blank control. The proliferation of each group of cells was measured by MTT assay. The apoptosis of cells in each group was detected by flow cytometry. The invasion ability of cells was detected by Transwell invasion assay. The expression of miR-193a-3p was detected by real-time quantitative PCR. blot detection of anti-apoptotic factor myeloid leukemia gene (Mcl-1) protein expression. Results Compared with group B and group C, the proliferation rate of group A was decreased (P <0.05) and the apoptosis rate of group A was increased (P <0.05) 48 h after transfection. The number of cells passing through polycarbonate membrane decreased <0.01). The expression of miR-193a-3p increased (P <0.05) and the expression of Mcl-1 decreased (P <0.05). Conclusion miR-193a-3p may inhibit the proliferation and invasion of Hep-2 cells and promote its apoptosis by regulating the expression of Mcl-1 gene in Hep-2 cells.