Fig. 5

AL139294.1 promotes the tumorigenic capacities of the NSCLC cells by indirectly regulating BRD4 and activating the Wnt and NF-κB2 pathways. A Schematic diagram represents the predicted binding sites of miR-204-5p with wild-type and mutant AL139294.1. B Luciferase assay was conducted to examine the binding of miR-204-5p mimics with wild-type or mutant AL139294.1 in HEK-293T cells. C The effects of AL139294.1 knockdown, and the co-transfection of si202 with miR-204-5p inhibitors on the proliferation ability of Beas-2B and NCI-H1299 cells were examined by CCK-8 assay. Wound healing assay (D) and transwell assay (E) were used to evaluate the migration and invasion of Beas-2B and NCI-H1299 cells transfected with AL139294.1 si202 and miR-204-5p inhibitors. F Western blotting was carried out to test BRD4 and EMT-related proteins after the transfection of AL139294.1 si202 and miR-204-5p inhibitors. G Colony formation assay was performed to evaluate the colony formation ability of cells. H The mRNA levels of BRD4 in cells were detected by qPCR after the transfection of AL139294.1 si202 and miR-204-5p inhibitors. I TCGA-LUADLUSC dataset reveals the positive correlation of BRD4 mRNA with Wnt5a and NF-κB2 mRNAs in lung cancer tissues. J Western blotting was used to detect the levels of Wnt5a pathway-related proteins (Wnt5a, β-catenin, AKT, and JNK) and NF-κB2 pathway-related proteins (NF-κB2, and SPP1) in Beas-2B and NCI-H1299 cells treated with AL139294.1 si202, miR-204-5p inhibitors or JQ1. *P < 0.05, **P < 0.01