Objective To investigate the effects of the long non-coding RNA FEZF1-AS1(LncRNA FEZF1-AS1)on the proliferation,migration,invasion,and epithelial-mesenchymal transition(EMT)of cells in idiopathic pulmonary fibrosis(IPF)and its underlying mechanisms.Methods A549 cells were treated with Transforming growth factor-β1(TGF-β1)to induce a pulmonary fibrosis cell model,dividing them into a blank control group(A549 cell group)and a model group.Western blotting was used to measure the expression of E-cadherin,N-cadherin,and Vimentin to verify the model's success.Real-time quantitative polymerase chain reaction(qRT-PCR)was employed to measure the expression of LncRNA FEZF1-AS1 and microRNA-200c-3p(miR-200c-3p).Based on experimental goals and different transfection plasmids,A549 cells were divided into three groups:Blank,TGF-β1+Si LncRNA FEZF1-AS1 NC,and TGF-β1+Si LncRNA FEZF1-AS1.Cell proliferation was evaluated using the CCK-8 assay,migration was assessed with wound healing assays,and invasion capabilities were measured using Transwell assays.Western blotting and qRT-PCR were repeated to assess protein and gene expression changes.Results In the model group,the relative expression of E-cadherin decreased,while N-cadherin and Vimentin increased compared to the blank control(P＜0.05).LncRNA FEZF1-AS1 was upregulated,and miR-200c-3p was downregulated in the model group compared to the control(P＜0.05).Compared to the Blank group,cell proliferation,migration,and invasion were increased in the TGF-β1+Si LncRNA FEZF1-AS1 NC group(P＜0.05).In contrast,these parameters were reduced in the TGF-β1+Si LncRNA FEZF1-AS1 group compared to the NC group(P＜0.05).Also,this group showed decreased expression of LncRNA FEZF1-AS1,N-cadherin,Vimentin,and increased E-cadherin compared to the NC group(P＜0.05).The expression of miR-200c-3p was higher in the TGF-β1+Si LncRNA FEZF1-AS1 and Blank groups compared to the NC group(P＜0.05).Conclusions LncRNA FEZF1-AS1 promotes the proliferation,migration,invasion,and EMT processes in pulmonary fibrosis cells by inhibiting miR-200c-3p.
维普
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