【摘要】 目的观察miR-409-3p对非小细胞肺癌细胞系A549增殖的影响及其机制。方法对照组为常规条件下培养的转染阳性对照核苷酸的A549细胞寡核苷酸组。实验组在对照组的基础上采用化学合成miR-409-3p模拟物,脂质体转染构建miR-409-3p高表达A549细胞;经q PCR检测,观察2组48 h后miR-409-3p的表达; MTT法检测细胞增殖;流式细胞计量术检测细胞凋亡和周期的差异。结果 miR-409-3p模拟物转染后,A549细胞中miR-409-3p表达水平显著升高(P<0. 05);细胞总凋亡比例为22. 66%±4. 61%,显著高于对照组的7. 78%±1. 95%(P<0. 05); G0/G1期为40. 21%±5. 37%,显著低于对照组细胞56. 09%±5. 22%(P<0. 05);双荧光报告系统表明癌基因ELF2是miR-409-3p的靶基因,过表达miR-409-3p模拟物后,内源性ELF2蛋白表达水平显著下降(P<0. 05)。结论 miR-409-3p可能通过调控ELF2的转录水平抑制非小细胞肺癌细胞A549增殖并促进其凋亡。更多还原

【Abstract】 Objective To detect the effects of miR-409-3 p on the proliferation of non-small-cell lung cancer cell line A549. Methods The control group was A549 cells of human non-small cell lung cancer cell line cultured under normal conditions transfected with contrast oligonucleotides. On the basis of the control group,the experimental group used chemical synthesis miR-409-3 p mimetic and liposome transfection to construct miR-409-3 p high-expression lung cancer A549 cells; The expression of miR-409-3 p,cell proliferation by MTT,apoptosis and cycle after48 h were observed by flow cytometry. Results The expression of miR-409-3 p mimic increased significantly in A549 cells after transfection,but decreased significantly in the control group. The percentage of total apoptosis was22. 66%±4. 61%,which was significantly higher than that of the control group 7. 78% ± 1. 95 %( P < 0. 05) : The G0/G1 phase was 40. 21% ± 5. 37%,significantly lower than the control group cells 56. 09% ± 5. 22%( P<0. 05).The double fluorescence reporting system showed that the oncogene ELF2 was the target gene of miR-409-3 p. After the expression of miR-409-3 p mimic,the endogenous ELF2 protein expression decreased significantly. Conclusions miR-409-3 p may inhibit the proliferation and promote apoptosis of non-small cell lung cancer cells A549 by regulating the transcription of ELF2.更多还原