目的 研究FEZ家族锌指1-反义 RNA 1(LncRNA FEZF1-AS1)对肺间质纤维化细胞增殖、侵袭能力及上皮间质转化（EMT）的影响及其作用机制。方法 采用转化生长因子β1(TGF-β1) 作用于A549细胞诱导肺间质纤维化细胞模型，将其分为A549细胞组（空白对照组）和造模组，采用Western blotting法检测各组中E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）及波形蛋白（Vimentin）的蛋白表达水平观察造模是否成功。采用实时荧光定量PCR（qRT-PCR）法检测两组中LncRNA FEZF1-AS1和miR-200c-3p基因的表达。根据实验目的和转染质粒的不同，将A549细胞分为空白对照（blank）组、TGF-β1+Si LncRNA FEZF1-AS1 NC组、TGF-β1+Si LncRNA FEZF1-AS1组，采用CCK-8法检测各组细胞增殖能力、采用细胞划痕检测各组细胞迁移能力、采用Transwell检测细胞侵袭能力；采用Western blotting法检测各组中E-cadherin、N-cadherin及Vimentin的蛋白表达水平；采用qRT-PCR法检测各组中LncRNA FEZF1-AS1和miR-200c-3p的基因表达水平。结果 造模组与对照组比较，E-cadherin的蛋白表达水平减少（P＜0.05）；N-cadherin及Vimentin的蛋白表达水平升高（P＜0.05）；造模组与对照组比较，LncRNA FEZF1-AS1基因的表达水平升高（P＜0.05），miR-200c-3p基因表达水平降低（P＜0.05）；与blank组比较，TGF-β1+Si LncRNA FEZF1-AS1 NC组细胞增殖、迁移、侵袭能力高于blank组（P＜0.05）；与TGF-β1+Si LncRNA FEZF1-AS1 NC组比较，TGF-β1+Si LncRNA FEZF1-AS1组细胞增殖、侵袭、迁移能力降低（P＜0.05）；与TGF-β1+Si LncRNA FEZF1-AS1 NC组比较，TGF-β1+Si LncRNA FEZF1-AS1组LncRNA FEZF1-AS1基因表达及N-cadherin、Vimentin蛋白表达降低，E-cadherin蛋白表达升高；与TGF-β1+Si LncRNA FEZF1-AS1 NC组比较，TGF-β1+Si LncRNA FEZF1-AS1组和blank组miR-200c-3p基因表达升高（P＜0.05）。结论 LncRNA FEZF1-AS1通过抑制miR-200c-3p促进肺间质纤维化细胞增殖、侵袭、转移和EMT过程。
Objective to investigate the effects of FEZ family zinc finger 1-antisense RNA 1(LncRNA FEZF1-AS1) on the proliferation, invasion and epithelial interstitial transition (EMT) of pulmonary fibrosis cells and its mechanism. Methods Transforming growth factor β1(TGF-β1) was applied to A549 cells to induce pulmonary interstitial fibrosis cell models, which were divided into A549 cells group (blank group) and model group. The protein expression levels of E-cadherin, N-cadherin and Vimentin in each group were detected by western blotting method to observe whether the modeling was successful. The expressions of LncRNA FEZF1-AS1 and miR-200c-3p in the two groups were detected by Quantitative Real-time PCR (qRT-PCR). According to the experimental purpose and transfection plasmid, the cells were divided into blank group, TGF-β1+Si LncRNA FEZF1-AS1 NC group, TGF-β1+Si LncRNA FEZF1-AS1 group. Cell proliferation ability was detected by CCK-8 method, cell migration ability was detected by cell scratch, and cell invasion ability was detected by Transwell assays. The protein expressions levels of E-cadherin, N-cadherin and Vimentin in each group were detected by western blotting. LncRNA FEZF1-AS1 and miR-200c-3p gene expression levels in each group were detected by qRT-PCR. Results Compared with the blank group, the protein expression level of E-cadherin in the modeling group was decreased (P < 0.05)，and the protein expression levels of N-cadherin and Vimentin were increased (P < 0.05). Compared with the blank group, the expression level of LncRNA FEZF1-AS1 gene in the modeling group was increased (P < 0.05), and the expression level of miR-200c-3p gene was decreased (P < 0.05). Compared with blank group, the proliferation, migration and invasion ability of TGF-β1+Si LncRNA FEZF1-AS1 NC group were higher (P < 0.05). Compared with TGF-β1+Si LncRNA FEZF1-AS1 NC group, the cell proliferation, invasion and migration ability of TGF-β1+Si LncRNA FEZF1-AS1 group were decreased (P < 0.05). Compared with TGF-β1+Si LncRNA FEZF1-AS1 NC group, LncRNA FEZF1-AS1 gene expression and protein expressions of N-cadherin and Vimentin were decreased in TGF-β1+Si LncRNA FEZF1-AS1 group, and the expression of E-cadherin protein was increased. Compared with TGF-β1+Si LncRNA FEZF1-AS1 NC group, the expression of miR-200c-3p gene in TGF-β1+Si LncRNA FEZF1-AS1 and blank groups were increased (P < 0.05). Conclusions LncRNA FEZF1-AS1 can promote the proliferation, invasion, metastasis and EMT process of pulmonary interstitial fibrosis cells by inhibiting miR-200c-3p.