AIM:To investigate the mechanism of microRNA-138-5p (miR-138-5p) inhibiting the proliferation,migration and invasion abilities of lung cancer cells.METHODS:The lung cancer A549 and H460 cells were transfected with miR-NC (control group) or miR-138-5p (experimental group).The bioinformatic analysis was performed to predict the target genes of miR-138-5p.The expression levels of miR-138-5p,forkhead box protein C1 (FOXC1) mRNA and vimentin mRNA were detected by RT-qPCR.The protein expression of FOXC1,vimentin,E-cadhcrin,N-cadherin and β-catenin was determined by Western blot.MTS method and colony formation assay were used to detect cell viability and proliferation ability.Wound healing assay and Transwell assay were used to detect cell migration and invasion ability.RESULTS:Over-expression of miR-138-5p significantly reduced the expression of FOXC1 and vimentin at mRNA and protein levels (P ＜ 0.05).The expression of E-cadherin and β-catenin were up-regulated and the expression of N-cadherin was down-regulated.The proliferation,migration and invasion abilities of the lung cancer cells were inhibited by the over-expression of miR-138-5p.CONCLUSION:miR-138-5p inhibits the proliferation,migration and invasion abilities of lung cancer cells by targeting FOXC1 and vimentin.It may be a potential target for lung cancer gene therapy.%目的:探讨微小RNA-138-5p(miR-138-5p)抑制肺癌细胞增殖、迁移和侵袭能力的相关机制.方法:以肺癌细胞A549和H460作为研究对象,分别转染miR-NC(对照组)或miR-138-5p(实验组);生物信息学技术预测miR-138-5p的靶基因;RT-qPCR检测转染后细胞miR-138-5 p、叉头框蛋白C1(FOXC1) mRNA和波形蛋白(vi-mentin) mRNA的相对表达量;Western blot法检测FOXC1、vimentin、E-cadherin、N-cadherin和β-catenin蛋白表达变化;MTS法和集落形成实验分别检测细胞的增殖能力;划痕愈合实验和Transwell法检测细胞迁移和侵袭能力.结果:miR-138-5p过表达显著降低FOXC1和vimentin的mRNA及蛋白的表达(P＜0.05),E-cadherin和β-catenin蛋白表达上调,N-cadherin蛋白表达下调,显著抑制肺癌细胞的增殖、迁移和侵袭能力(P＜0.05).结论:miR-138-5p可以通过靶向干扰FOXC1和vimentin的表达抑制肺癌细胞的增殖、迁移和侵袭,可能是肺癌基因治疗的潜在靶点.
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