To investigate the effect on β-Catenin pathway by lncRNA urothelial carcinoma associated 1 (UCA1) targeting regulated miR-185-5p in human lung adenocarcinoma A549 cell line.A549 cell was selected as the study model and were divided into four groups, blank control group, sh-scramble negative control group (sh-scramble), sh- interference group (sh-), miR-185 inhibitor group (miR-185 inhibitor) and sh-+ inhibitor group (sh-+inhibitor). The proliferation-, apoptosis- and autophagy- related protein levels were determined by Western blot. qRT-PCR was employed to detect the mRNA levels of and miR-185-5p. The relationship between lnRNA and miR-185-5p was validated by bioinformatics analysis and luciferase reporter system assays. BrdU staining was used to detect the cell growth, and immunofluorence staining was performed to measure the content of LC3 cells.sh- significantly decreased expression and increased miR-185-5p expression in A549 cells, and inhibited the cell growth and autophagy, while promoted the cell apoptosis (<0.01). Bioinformatics analysis and luciferase reporter system assays demonstrated that lncRNA and miR-185-5 can combine effectively, indicating that they have a targating relationship. sh- also significantly inhibited the protein levels of β-Catenin/TCF-4, Beclin 1 and LC3 Ⅱ, and decreased the cell growth and autophagy by the miR-185-5p; and down-regulated the LC3 expression (<0.01).The effect of inhibition for miR-185-5p was decreased by lncRNA inference, and released the β-Catenin/TCF-4, Beclin 1 and LC3 Ⅱ, and further reduced the autophagy and growth in A549 cells.