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目的探讨miR-125a在肺癌细胞增殖凋亡侵袭中的作用。方法以肺癌细胞A549、NCL-H661、NCL-H460、SPC-A-1和支气管上皮细胞HBE为研究对象,提取细胞RNA,反转录合成miR-125a的cDNA,RT-PCR检测细胞中miR-125a的表达水平。转染miR-125a inhibitor、inhibitor control、miR-125a mimics、mimics control到细胞A549中,MTT法检测细胞增殖情况,原位末端标记法检测细胞凋亡情况,Transwell小室检测细胞侵袭力。结果 miR-125a表达水平按照由大到小的顺序依次为:HBE、SPC-A-1、NCL-H460、NCL-H661、A549细胞,肺癌细胞中miR-125a表达水平均低于支气管上皮细胞HBE。miR-125a inhibitor组比inhibitor control组抑制率低(P<0.01);miR-125a mimics组比mimics control组抑制率高(P<0.01)。miR-125a inhibitor组比inhibitor control组凋亡率低(P<0.05),miR-125a mimics组比mimics control组凋亡率高(P<0.01)。miR-125a inhibitor组侵袭力比inhibitor control侵袭力强(P<0.01);miR-125a mimics组侵袭力比mimics control侵袭力低(P<0.01)。结论 miR-125a在肺癌细胞A549、NCL-H661、NCL-H460、SPC-A-1中低表达,miR-125a可抑制细胞增殖,促进细胞凋亡,降低细胞侵袭力。
Objective To investigate the role of miR-125a in the proliferation and apoptosis of lung cancer cells. METHODS: Human lung adenocarcinoma A549, NCL-H661, NCL-H460, SPC-A-1 and bronchial epithelial cell line HBE were used as research objects. RNA was extracted and the cDNA of miR-125a was reverse transcribed. RT- 125a expression levels. The cells were transfected with miR-125a inhibitor, inhibitor control, miR-125a mimics and mimics control. Cell proliferation was detected by MTT assay. Cell apoptosis was detected by in situ terminal labeling. Results The expression levels of miR-125a in lung cancer cells were lower than those in bronchial epithelial cells HBE, SPC-A-1, NCL-H460, NCL-H661 and A549 cells in descending order . The inhibition rate of miR-125a inhibitor group was lower than that of inhibitor control group (P <0.01). The inhibition rate of miR-125a mimics group was higher than that of mimics control group (P <0.01). The apoptosis rate of miR-125a inhibitor group was lower than that of inhibitor control group (P <0.05), and the apoptosis rate of miR-125a mimics group was higher than that of mimics control group (P <0.01). The invasiveness of miR-125a inhibitor group was higher than that of inhibitor control (P <0.01). The invasiveness of miR-125a mimics group was lower than that of mimics control (P <0.01). Conclusion miR-125a is low expressed in lung cancer cell lines A549, NCL-H661, NCL-H460 and SPC-A-1. MiR-125a can inhibit cell proliferation, promote cell apoptosis and decrease cell invasiveness.