Fig. 6.

MiR-199a-5p is the intermediate downstream of LINC01123 that increases c-Myc level. a Schematic representation of the predicted binding site between miR-199a-5p and LINC01123 in wild-type and mutant-type was shown. b MiR-199a-5p mRNA level was negatively regulated by LINC01123 in A549 and H1299 cells. c The relative luciferase activity of 293 T cell was tested after co-transfection with LINC01123 wide-type and miR-199a-5p mimics. d Schematic representation of the predicted binding site between miR-199a-5p and c-Myc mRNA 3′-UTR in wild-type and mutant-type was shown. e, f LINC01123 mRNA level and c-Myc mRNA and protein levels were downregulated by miR-199a-5p mimics and upregulated by miR-199a-5p inhibitor in A549 and H1299 cells. g, h Rescue experiment of c-Myc mRNA and protein expression by co-transfection of 1123-OE pcDNA and miR-199a-5p mimics in A549 cell, or co-transfection of si-1123 and miR-199a-5p inhibitor in H1299 cell. i The dual-luciferase activity assay in 293 T cell demonstrated that miR-199a-5p mimics could significantly reduce the luciferase activity of wild-type but not mutant-type c-Myc 3′-UTR, and the reduction of luciferase activity could be restored by ectopic expression of LINC01123. MiR-199a-5p inhibitor slightly increased the luciferase activity of wild-type c-Myc 3′-UTR, but co-transfected with si-1123 reversed the luciferase activity. j A RIP assay was performed using anti-normal mouse IgG or anti-Ago2 in A549 cell lysates. The relative expression levels of LINC01123 and miR-199a-5p were detected by qRT-PCR. Data shown are mean ± SD (n = 3) (*P < 0.05, **P < 0.01, ***P < 0.001)