Fig. 6.

Knockdown of EGFR alleviates the proliferative effects of anti-miR-1231 on glioma cell tumorigenesis in vitro. a Western blotting assay showing suppression of upregulated EGFR and downstream PI3K/AKT signaling pathway proteins in miR-1231-silenced cells transfected with siRNAs against EGFR. GAPDH was used as the loading control. Data are presented as the means of triplicate experiments. b Cell viability determined by transfection of siRNA-EGFR into LN229, U251, and PG1 cells with anti-miR-1231. Experiments were performed three times using triplicate samples, *P < 0.05, **P < 0.01. c, d Colony formation analysis of glioma cells infected with si-NC or si-EGFR, followed by transfection of anti-miR-1231 or negative control. Experiments were performed three times using triplicate samples, *P < 0.05, **P < 0.01. e, f Cell growth analyzed using the EDU assay 48 h after co-transfection, *P < 0.05, **P < 0.01. g, h Cell cycle results of LN229, U251, and PG1 glioma cells transfected with si-NC or si-EGFR in the presence or absence of anti-miR-NC or anti-miR-1231 for 72 h