Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

Figure 4

MEG3 interacts with miR-6088 to regulate SMARCB1. Note: pcDNA3.1, pcDNA3.1-MEG3, si-NC, or si-MEG3 plasmid was transfected into U87 and U251 cells. RT-PCR was applied to detect miR-6088 expression (a). Starbase predicted the binding sites of MEG3 and miR-6088, and the mutation sites of MEG3 were designed (b). HEK-293T cells were transfected or cotransfected with mimic NC, miR-6088 mimic, inhibitor NC, or miR-6088 inhibitor with WT-SMARCB1 or MT-SMARCB1. Fluorescent activity was surveyed by dual-luciferase reporter gene (c). Mimic NC, miR-6088 mimic, inhibitor NC, or miR-6088 inhibitor was transfected into U87 and U251 cells, and qRT-PCR was applied to detect the transfection efficiency of the overexpression and inhibition of miR-6088 (d) in U87 and U251 cells. SMARCB1 mRNA (e) and protein expression levels (f) were surveyed by RT-PCR and Western blot, respectively. Starbase predicted the binding site of miR-6088 and SMARCB1. The mutation site of SMARCB1 was designed (g). HEK-293T cells were transfected or cotransfected with mimic NC, miR-6088 mimic, inhibitor NC, or miR-6088 inhibitor with WT-SMARCB1 or MT-SMARCB1. Fluorescent activity was surveyed by dual-luciferase reporter gene assay (h). , , .

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