Fig. 7

STAT1 increases ovarian surface epithelial cell proliferation, migration, and invasion. a HOSEpiC, OVCAR-3, and SK-OV-3 cells were transiently transfected with STAT1α or STAT1β plasmid in the absence or presence of TGF-β1 (10 ng/ml) for 48 h. Cell proliferation was measured by the WST-1 assay. pcDNA4 was used as negative control. Different superscript denotes statistically significant difference (P < 0.05; n = 3 independent experiments). b HOSEpiC, OVCAR-3, and SK-OV-3 cells were transiently transfected with STAT1-siRNA or non-specific control (NC)-siRNA. Cell proliferation was measured by the WST-1 assay at 48 h post-transfection (*, P < 0.05; n = 3 independent experiments). c Wound healing assay in SK-OV-3 cells after transiently transfecting with STAT1α or STAT1β plasmid for 24, 48, and 72 h. d Quantitative analysis of the wound width in (c). e Wound healing assay in SK-OV-3 cells after transiently transfecting with STAT1-siRNA (STAT1-siR) for 24, 48, and 72 h. f Quantitative analysis of the wound width in (e). STAT1 promotes the migration of SK-OV-3 cells. Original magnification, × 200; scale bars, 500 μm. g Invasion assay of SK-OV-3 cells after transiently transfecting with STAT1α or STAT1β plasmid for 48 h. h Quantitative analysis of invaded cells in (g). i Invasion assay of SK-OV-3 cells after transiently transfecting with STAT1-siRNA or NC-siRNA for 48 h. j Quantification analysis of invaded cells in (i). Invaded cells were counted from three random fields. STAT1 promotes the invasion of SK-OV-3 cells. Original magnification, × 200; scale bar, 500 μm. Data are presented as the mean ± standard deviation (SD). *, P < 0.05 compared to control