Effects of Interference with UCA1 and Inhibition of miR-185-5p on Activation,Autophagy and Survival of β-Catenin Pathway in Non-small Cell Lung Cancer

ObjectiveTo 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. MethodsA549 cell was selected as the study model and were divided into four groups,blank control group,sh-scramble negative control group (sh-scramble),sh-UCA1 interference group (sh-UCA1),miR-185 inhibitor group (miR-185 inhibitor) and sh-UCA1+ inhibitor group (sh-UCA1+inhibitor). The proliferation-,apoptosis- and autophagy- related protein levels were determined by Western blot. qRT-PCR was employed to detect the mRNA levels of UCA1 and miR-185-5p. The relationship between lnRNA UCA1 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. Resultssh-UCA1 significantly decreased UCA1 expression and increased miR-185-5p expression in A549 cells,and inhibited the cell growth and autophagy,while promoted the cell apoptosis (P<0.01). Bioinformatics analysis and luciferase reporter system assays demonstrated that lncRNA UCA1 and miR-185-5 can combine effectively,indicating that they have a targating relationship. sh-UCA1 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 (P<0.01). ConclusionThe effect of UCA1 inhibition for miR-185-5p was decreased by lncRNA UCA1 inference,and released the β-Catenin/TCF-4,Beclin 1 and LC3 Ⅱ,and further reduced the autophagy and growth in A549 cells.