RESUMEN
Objective To determine the expression levels of zinc finger antisense 1 (ZFAS1) in tumor tissues of non-small cell lung cancer (NSCLC) and investigate the biological roles of ZFAS1 in NSCLC.Methods The relative expression levels of ZFAS1 in tumor tissues of NSCLC patients were determined by using real-time fluorescent qRT-PCR.RNA interference was used to knock down ZFAS1 expression in A549 cells.The proliferations of A549 cells with ZFAS1 knockdown were determined by cell counting and cell colony formation assays.Flow cytometric analysis was used to determine the cellular cycle distribution and apoptosis of the A549 cells with ZFAS1 knockdown.Transwell migration and matrigel invasion assays were used to determine the migration and invasion of the A549 cells with ZFAS1 knockdown.The gene expression levels of cyclin D1,Bcl2,N-cadherin,ZEB1,Slug and Twist were determined by real-time fluorescent qRT-PCR.Results The mean expression levels of ZFAS1 in tumor tissues of NSCLC patients [0.01 (0.002 to 0.054)] were significantly higher than those in the adjacent non-cancerous tissues [0.002 (0.001 to 0.012)] (Z =-2.638;P ＜ 0.01).After ZFAS1 knockdown,the proliferation of A549 cells was remarkably retarded (P ＜ 0.01).The percentage of cells at G1 phase was increased while the cells at S phase was decreased (P ＜ 0.01).The rate of apoptotic cells was significantly increased in A549 cells with ZFAS1 knockdown (P ＜ 0.01).A549 cells showed decreased migration and invasion abilities after ZFAS1 knockdown (P ＜0.01).The expression levels of cyclin D1,Bcl2,N-cadherin,ZEB1,Slug and Twist genes were decreased in ZFAS1 knockdown A549 cells (P ＜ 0.05).Conclusion ZFASI was highly expressed in the tumor tissues of NSCLC patients.ZFAS1 knockdown induced cell cycle arrest,cell apoptosis and suppression of epithelial-mesenchymal transition (EMT),leading to the inhibition of proliferation,migration,and invasion of NSCLC cells.