Fig. 3

PI3 Kα isoform is required for Wnt5a-induced RhoA activity. a, c Human osteosarcoma cells MG-63 (a) and U20S (c), serum-deprived for 24 h, were pre-treated with 10 µmol/L LY294002 (PI3K inhibitor) for 1 h, were incubated with 100 ng/mL Wnt5a and harvested at 30 min after the start of Wnt5a treatment. The relative RhoA activity was normalized to the average value of LY294002/Wnt5a-untreated group. b, d Serum-deprived MG-63 (b) and U20S cells (d) were pre-treated with 1 nmol/L HS-173 (PI3Kα inhibitor), 10 nmol/L TGX-221 (PI3Kβ inhibitor), 10 nmol/L CZC24832 (PI3Kγ inhibitor) and 10 nmol/L CAL-101 (PI3Kδ inhibitor) for 1 h, then were incubated with 100 ng/mL Wnt5a and harvested at 30 min after the start of Wnt5a treatment. Data were presented as mean ± SD of 3 determinations. The relative RhoA activity was normalized to the average value of each inhibitor-untreated group