Fig. 6: The RhoA-mediated signaling pathway participated in sphingosine-1-phosphate receptor 1 (S1PR1)-mediated vasculogenic mimicry (VM) and endothelium-dependent vessel (EDV).
From: S1PR1 regulates the switch of two angiogenic modes by VE-cadherin phosphorylation in breast cancer
a RhoA measurement in the different treatment groups by G-LISA. b, c The protein levels of S1PR1, VE-cadherin, VE-cadherin (Y731), and β-catenin and RhoA activation in MCF-7 cells after treatment with various RhoA inhibitor concentrations for 24 h. Treatment with 2 µl/ml of the RhoA inhibitor was the optimum concentration. d After treatment with 2 µl/ml of the RhoA inhibitor, the S1PR1, VE-cadherin, VE-cadherin (Y731), and β-catenin protein levels in the control or shS1PR1 MCF-7 cells are shown. e The RhoA inhibitor restrained vascular endothelial growth factor (VEGF) secretion by MCF-7 cells. f, g The RhoA inhibitor induced VM channel formation (100 × , bar 50 µm) and inhibited the number of EDVs in MCF-7 cells in 3D culture (40 × , bar 100 µm). h After treatment with the RhoA inhibitor, the S1PR1, VE-cadherin and β-catenin protein levels changed, as shown by immunofluorescence staining (100 × , bar 50 µm). The mean ± SD is shown. *p < 0.05 (n = 3)
