Fig. 5

SNHG1 promoted the expression of FOXP2 by inhibiting miR-154-5p and miR-376b-3p, further enhancing the expression level of KDM5B. a Western blot analysis on FOXP2 and KDM5B in SNHG1-knockdown glioma cells. **P < 0.01 vs. sh-NC group. b Western blot analysis revealed the negative correlation between miR-154-5p or miR-376b-3p and KDM5B expression in U87 and U251 cells. **P < 0.01 vs. pre-NC group, ^##P < 0.01 vs. anti-NC group. c SNHG1 knockdown and miR-154-5p or miR-376b-3p overexpression decreased the protein expression of FOXP2 and KDM5B in U87 and U251 cells. **P < 0.01 vs. sh-NC + pre-NC group, ^##P < 0.01 vs. sh-SNHG1 + pre-miR-154-5p group, ^∆∆P < 0.01 vs. sh-SNHG1 + pre-miR-376b-3p group. d FOXP2–3′-UTR-Wt reversed overexpression of miR-154-5p and miR-376b-3p induced attenuation of FOXP2 and KDM5B expression in U87 and U251 cells. **P < 0.01 vs. pre-NC + FOXP2-NC group, ^##P < 0.01 vs. pre-miR-154-5p + FOXP2-NC group, ^∆∆P < 0.01 vs. pre-miR-376b-3p + FOXP2-NC group. e Western blot analysis of the PI3K/AKT pathway regulated by KDM5B in U87 and U251 cells. **P < 0.01 vs. sh-NC group. Data above were presented as the mean ± SD (n = 5, each group). GAPDH was used as an endogenous control