Objective To detect the expression of DCST1-AS1 in non-small cell lung cancer and explore its effect on malignant biological behavior of cancer cells.Methods The tissues and corresponding adjacent tissues from 65 patients with non-small cell lung cancer were collected,and the normal human bronchial epithelial cells 16HBE and the non-small cell lung cancer cell lines(A549,H1299,H1650 and HCC827)were cultured in vitro.The expression levels of DCST1-AS1 and miR-29b in tissues and cells were detected by RT-qPCR assay,and the correlation between the DCST1-AS1 expression and the clinical characteristics of patients with non-small cell lung cancer were analyzed.A549 cells were divided into the control group,the si-NC group,the si-DCST1-AS1 group,the si-DCST1-AS1+ anti-NC group and the si-DCST1-AS1+anti-miR-29b group.The cell proliferation was detected by CCK-8 assay and clone formation assay,the invasion and migration of cells were detected by Transwell;the expression of E-cadherin,Vimentin and N-cadherin was detected by Western blot.Results The expression of DCST1-AS1 increased and the expression of miR-29b decreased in non-small cell lung cancer tissues and cells(P<0.05).The expression of DCST1-AS1 was correlated with TNM stage,differentiated degree of tissue,lymph node metastasis and pathological types in non-small cell lung cancer patients(P<0.05).Compared with the control group or the si-NC group,the expression of DCST1-AS1,OD value,number of colony-forming cells,migration cells and invasion cells and the expression of Vimentin and N-cadherin in A549 cells of the si-DCST1-AS1 group decreased(P<0.05),while the expression of miR-29b and E-cadherin increased(P<0.05).Knocking down miR-29b could significantly reduce the effect of down-regulation of DCST1-AS1 expression on the malignant biological behavior of A549 cells.Conclusion DCST1-AS1 is highly expressed in non-small cell lung cancer,knocking down DCST1-AS1 may inhibit the malignant biological behavior of non-small cell lung cancer cells by up-regulating the expression of miR-29b.