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. 2019 Jul 1;20(3):2111–2118. doi: 10.3892/mmr.2019.10445

Figure 3.

Figure 3.

miR-29 regulates the PTEN/AKT signaling pathway in NPSCs. Single adhesive cultured NSPCs were transfected with (A) miR-29 mimic or (B) miR-29 inhibitor using Lipofectamine 2000. After transfection, NSPCs protein were collected at the end of each treatment and detected by western blot analysis after each time point (5, 15, 30, 60, 120 h). Data are presented as the mean ± standard deviation of three independent experiments. *P<0.05, **P<0.01, ***P<0.001 vs. 0 h. (C) To further investigate the effects of miR-29 on PTEN, the PTEN-specific inhibitor VO-OH was added to the medium before transfection and the medium after transfection still contained VO-OH. PTEN expression was quantified and normalized to β-actin. Data are presented as the mean ± standard deviation of three independent experiments. **P<0.01 vs. DMSO; ###P<0.001 vs. anti-miR-29. (D) Expression of p-AKT and AKT as determined by western blot analysis; p-AKT expression was normalized to total AKT expression. Data are presented as the mean ± standard deviation of three independent experiments. *P<0.05 vs. DMSO, ###P<0.001 vs. anti-miR-29. NSPC, neural stem/progenitor cell; miR-29, microRNA-29; anti-miR-29, miR-29 inhibitor; miR-NC, microRNA negative control; Ctrl, treatment with miRNA-free medium; DMSO, dimethyl sulfoxide; PTEN, phosphatase and tensin homologue deleted on chromosome 10; VO-OH, VO-OHpic trihydrate; p-, phosphorylated.