Fig. 7

miR-217 inhibited glioma cell malignant progression by regulating PI3K/AKT and ERK pathways via targeting HNF1β 3′-UTR. a CCK-8 assay was applied to determine the proliferation effect of miR-217 and HNF1β on U87 and U251 cells (data are presented as the mean + SD (n = 5, each group). Data are presented as the mean + SD (n = 5, each group). ^* P < 0.05 vs. miR-217+HNF1β group; ^# P < 0.05 vs. miR-217+HNF1β-NC group. b Quantification of migration and invasion cells with the expression of miR-217 and HNF1β changed. Representative images and accompanying statistical plots were presented (data are presented as the mean + SD (n = 5, each group). ^* P < 0.05 vs. miR-217+HNF1β group; ^# P < 0.05 vs. miR-217+HNF1β-NC group. Scale bars represent 40 μm). c Flow cytometry analysis of U87 and U251 with the expression of miR-217 and HNF1β changed (data are presented as the mean + SD (n = 5, each group). ^* P < 0.05 vs. miR-217+HNF1β group; ^# P < 0.05 vs. miR-217+HNF1β-NC group). d Western blot analysis of p-PI3K, PI3K, p-AKT, AKT, p-ERK, ERK, p-MEK1/2, and MEK1/2 regulated by miR-217 and HNF1β in U87 and U251 cells, they are shown using GAPDH as endogenous control (data are presented as the mean + SD (n = 5, each group). ^* P < 0.05 vs. miR-217+HNF1β group; ^# P < 0.05 vs. miR-217+HNF1β-NC group)