Downregulation of SLCO4C1 regulates the behavior of EC via the PI3K/Akt signaling pathway in HEC-1A and RL95-2 cells. (A) Expression of p-PI3K, PI3K, p-Akt and Akt in HEC-1A and RL95-2 cells from the Ctrl, siNC, siSLCO4C1-1 or siSLCO4C1-2 groups, as determined by western blotting. (B) Cell proliferation was detected by CCK-8 assay in HEC-1A and RL95-2 cells from the Ctrl, siNC, siSLCO4C1-1, siSLCO4C1-2, siSLCO4C1-1+740 Y-P (PI3K signaling activator) or siSLCO4C1-2+740 Y-P groups. (C) Cell apoptosis was detected by flow cytometry in HEC-1A and RL95-2 cells from the Ctrl, siNC, siSLCO4C1-1, siSLCO4C1-2, siSLCO4C1-1+740 Y-P or siSLCO4C1-2+740 Y-P groups. (D) Cell migration was detected by wound healing assay at 0 and 48 h in HEC-1A and RL95-2 cells from the Ctrl, siNC, siSLCO4C1-1, siSLCO4C1-2, siSLCO4C1-1+740 Y-P or siSLCO4C1-2+740 Y-P groups. (E) Expression of p-PI3K, PI3K, p-Akt and Akt in HEC-1A and RL95-2 cells from the Ctrl, siNC, siSLCO4C1-1, siSLCO4C1-2, siSLCO4C1-1+740 Y-P or siSLCO4C1-2+740 Y-P groups, as determined by western blotting. GAPDH was used as a loading control. The results were determined from triplicate experiments and the error bars represent the mean ± SD. Asterisks indicated a difference between siSLCO4C1 and siNC, whereas hashtags indicated a difference between siSLCO4C1+740 Y-P and siSLCO4C1. */#P<0.05, **/##P<0.01, ***/###P<0.001 vs. the Ctrl group and siNC group. SLCO4C1, solute carrier organic anion transporter family member 4C1; EC, endometrial cancer; p-PI3K, phosphorylated-PI3K; p-Akt, phosphorylated-Akt.