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目的:研究microRNA-224(miR-224)在人非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达及对NSCLC细胞增殖能力和凋亡的影响。方法:采用荧光实时定量PCR(q PCR)检测20对NSCLC组织与癌旁组织中miR-224的表达量,以及miR-224在NSCLC细胞A549与正常肺支气管上皮细胞中的表达量,并计算差值;转染anti-miR-224至A549细胞,q PCR检测anti-miR-224的转染效率;四甲基偶氮唑盐(MTT)实验及克隆形成实验检测miR-224对A549细胞增殖能力的影响,流式细胞技术检测细胞周期及凋亡;荧光素酶报告实验证实miR-224与靶基因Bim的结合;q PCR及Western blot检测转染anti-miR-224后A549细胞中Bim的表达量。结果:与癌旁正常组织相比,miR-224在NSCLC组织及细胞中均显著高表达(P<0.05);抑制miR-224能够显著抑制A549细胞的增殖能力并促进凋亡,并促进了Bim的表达。结论:miR-224在NSCLC中呈高表达,miR-224能够通过调控Bim抑制A549细胞的增殖能力并诱导凋亡。
Objective: To investigate the expression of miR-224 in human non-small cell lung cancer (NSCLC) and its effect on proliferation and apoptosis of NSCLC. Methods: The expression of miR-224 in 20 NSCLC tissues and adjacent normal tissues was detected by real-time quantitative PCR (qPCR) and the expression of miR-224 in NSCLC A549 and normal lung bronchial epithelial cells The transfection efficiency of anti-miR-224 was detected by q-PCR. MTT assay and colony formation assay were used to detect the proliferation of A549 cells . Flow cytometry was used to detect cell cycle and apoptosis. Luciferase reporter assay confirmed the binding of miR-224 to target Bim. The expression of Bim in A549 cells transfected with anti-miR-224 was detected by q-PCR and Western blot the amount. Results: miR-224 was highly expressed in both NSCLC tissues and cells (P <0.05), compared with the adjacent normal tissues. Inhibition of miR-224 significantly inhibited the proliferation and apoptosis of A549 cells and promoted the expression of Bim expression. CONCLUSION: miR-224 is overexpressed in NSCLC. MiR-224 can inhibit the proliferation of A549 cells and induce apoptosis by regulating Bim.