Fig. 4

SNCG induces ovarian cancer progression via activating the PI3K/AKT signaling pathway. a-b A phospho-kinase array kit was performed on protein lysates of SKOV3-sh1 and control cells. Thirteen proteins were obvious changes in their phosphorylation status and highlighted by boxes. c Western blot analysis of the levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in SKOV3 and HO-8901 PM cells transfected with SNCG-shRNA or Scr, and OVCAR3 cells transfected with SNCG-Ove or Ctrl. d Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, and DMSO were determined by Western blot. e Expression levels of Akt, p-Akt (Sec473), p70S6 kinase, p-p70S6 kinase (Thr389), mTOR, and p-mTOR (Sec2448) in cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, LY294002, and DMSO were determined by Western blot. f Wound healing assay (upper, original magnification × 40) and cell colony formation (lower) of cells transfected with SNCG shRNA, Scr, SNCG Ove, Ctrl, IGF-1, LY294002, and DMSO confirmed the effect of SNCG on the PI3K/AKT signaling pathway. ^▲, P < 0.05. *, P < 0.001. IGF-1: insulin-like growth factor 1; sh-SNCG: small hairpin RNAs of SNCG