Fig. 5

miR-26a activates the PI3K/Akt signaling pathway via down-regulation of PTEN. a the miR-26a binding site in PTEN 3’UTR; b detection of luciferase activity; c PTEN expression in glioma tissues and control brain tissues; d correlation analysis of miR-26a expression with PTEN expression; e PTEN protein expression in HBMECs transfected with miR-26a agomir or miR-26a antagomir; f Akt protein level and phosphorylation level in HBMECs transfected with PTEN overexpression vector and/or miR-26a agomir measured using Western blot analysis; *, p < 0.05, compared with NC mimic (b), control brain tissues (c), agomir-NC (e), or PTEN-NC (f) group; #, p < 0.05, compared with antagomir-NC or miR-26a agomir + PTEN-NC group; All data were expressed as mean ± standard deviation; there were 46 cases of glioma tissues and 28 cases of control brain tissues; the correlation analysis was conducted using Pearson correlation analysis; comparisons between two groups were analyzed using unpaired t-test; comparisons among multiple groups were analyzed by the one-way ANOVA; the experiment was repeated three times; ANOVA, analysis of variance; HBMECs, human brain microvascular endothelial cells; miR-26a, microRNA-26a; NC, negative control; PTEN, phosphatase and tensin homolog deleted on chromosome ten; Akt, protein kinase B; GAPDH, glyceraldehyde-3-phosphate dehydrogenase