Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p

Figure 2 miR-17-5p acted as the downstream molecule of circular RNA AKT3 to antagonize the effects of circular RNA AKT3 on TE-1 cells. A: Schematic of the miR-17-5p binding sites in wild-type (WT) circular RNA AKT3 (circAKT3) and the mutant (Mut) circAKT3 (up). Luciferase reporter assay was performed in HEK-293T cells to determine the binding ability between miR-17-5p and circAKT3 (down); B: The expression of miR-17-5p in tissue samples; C: CircAKT3 was negatively correlated with miR-17-5p in esophageal cancer tissue samples; D: miR-17-5p expression in indicated cell lines; E-H: Cell viability (E), migratory ability (F), invasive ability (G), and apoptosis (H) of circAKT3 overexpression (OE)-transfected TE-1 cells in the presence or absence of miR-17-5p mimics. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. HEEC: Human normal esophageal epithelial cell line; NC: Negative control; OD: Optical density.