Fig. 5

miR-155 regulated GC migration and invasion by targeting the SOX1 gene (a) Bioinformatics analysis of the possible binding sites between miR-155 and the SOX1 3′UTR. b miR-155 over-expression inhibited SOX1 RNA levels in SGC-7901 and MGC-803 cells. d miR-155 over-expression suppressed SOX1 protein levels in SGC-7901 and MGC-803 cells. miR-155 mimics were transfected into gastric cancer cells. Forty-eight hours after transfection, the mRNA levels were determined by RT-qPCR, and the protein levels were determined by Western-blot. GAPDH was used as a loading control. c miR-155 depletion with inhibitor upregulated SOX1 RNA levels in SGC-7901 and MGC-803 cells. e miR-155 depletion augmented SOX1 protein expression in SGC-7901 and MGC-803 cells. f miR-155 overexpression reduced SOX1 luciferase activity in SGC-7901 gastric cancer cells. g miR-155 depletion elevated SOX1 luciferase activity in SGC-7901 gastric cancer cells. h, i SOX1 and MRTF-A protein levels were determined by Western-blot in SGC-7901 cells and MGC-803 cells. j The effect of overexpressed or knocked down SOX1 on SGC-7901 migration of was detected by wound-healing assay. k Transwell assay was used to detect the migration-stimulating effects of overexpressed or knocked down SOX1 on SGC-7901. The number of cells that migrated to the lower side of the Transwell chamber was counted and photographed in five fields (the upper, lower, left, right, and middle fields) from three independent experiments, and the fold migration was calculated with the SPSS statistical software. Data are shown as the mean ± S.E.M based on three to six independent experiments. **, p < 0.01