Fig. 6

GOLM1 promotes human glioma progression through activation of AKT. a Image of phospho-kinase array performed with lysates prepared from U251-NC and -sh-GOLM1 cells. Spots with significant decreases in phosphorylation are numbered and quantification is shown in (b). c Western blot analysis of p-AKT (S473), AKT, p-ERK1/2, ERK1/2 in indicated cells. d Kinases and genes downstream of AKT in U251, A172 and U87MG cells were analyzed by western blot. U87MG-Lenti-NC and -Lenti-GOLM1 cells were treated with the AKT inhibitor MK-2206 (2 μM) or DMSO (vehicle control) and evaluated for e cell viability in the CCK8 assay and f cell proliferation in EdU (red) assays. Scale bar = 100 μm. g Graphic representation of ratios of EdU positive cells. Data are presented as the mean ± SEM. h Transwell migration and invasion assays were performed on U87MG-Lenti-NC and -Lenti-GOLM1cells with indicated treatment. i Quantification of invaded and migrated cells in Transwell assays after incubation for 24 h. Scale bar = 50 μm. (*P < 0.05 vs Lenti-NC + DMSO; **P < 0.01 vs Lenti-NC + DMSO; ***P < 0.001 vs Lenti-NC + DMSO; #P < 0.05 vs Lenti-GOLM1 + DMSO; ##P < 0.01 vs Lenti-GOLM1 + DMSO; ###P < 0.001 vs Lenti-GOLM1 + DMSO; $P < 0.05 vs Lenti-NC + MK-2206; $$$P < 0.001 vs Lenti-NC + MK-2206)