Fig. 3

LINC01116 facilitates LAD oncogenicity by sponging miR-744-5p. A, B LINC01116 distribution in A549 and PC9 was explored by subcellular fractionation and FISH assays. Student’s t test was applied for analysis. C It was mirrored in RNA pull down assays that miR-744-5p was much enriched by Biotin LINC01116-WT. One-way ANOVA was applied for analysis. D Binding sites of miR-744-5p and LINC01116 were predicted. E Calculation of miR-744-5p expression in LAD cells and HBE was achieved by means of qRT-PCR. One-way ANOVA was applied for analysis. F LINC01116 fragment covering the wild-type or mutated miR-744-5p interacting sequences was inserted into pmirGLO luciferase vector. Luciferase activities were normalized to renilla luciferase. Student’s t test was applied for analysis. G RNA pull down verified the interaction between LINC01116 and miR-744-5p. One-way ANOVA was applied for analysis. H qRT-PCR analysis was applied for determining the efficiency of miR-744-5p inhibitor. Student’s t test was applied for analysis. I–M Function experiments and rescue assays were performed for detecting miR-744-5p influences on LAD and the rescuing effects of miR-744-5p inhibitor on suppressed cell malignant behaviors induced by LINC01116 knockdown. Student’s t test was applied for analysis between NC inhibitor and miR-744-5p inhibitor or between NC mimics and miR-744-5p mimics, while one-way ANOVA was applied for analysis among sh-NC, sh-LINC01116#1 and sh-LINC01116#1  +  miR-744-5p inhibitor. *P  <  0.05, **P  <  0.01