Fig. 5

miR-490-3p inhibited TGFβ1-induced EMT through directly targeting TGFβR1. a Diagram of bioinformatic prediction of binding site of TGFβR1 by miR-490-3p. b Cells were cotransfected with scrambled RNA or miR-490-3p together with TGFβR1-3′-UTR or TGFβR1-mut-3′-UTR luciferase reporter in the presence of firefly luciferase reporter plasmid. Renilla luciferase activity and firefly luciferase activity were measured by dual-luciferase reporter assay. Renilla luciferase activity was normalized to firefly luciferase activity. c The mRNA level of TGFβR1 in ovarian cancer cells (SKOV3 and CaOV3) transfected with negative control, miR-490-3p mimics, miR-490-3p mimics plus TGFβR1 was detected by RT-qPCR analysis. d Westernblot analysis showed the protein level of TGFβR1 in ovarian cancer cells (SKOV3 and CaOV3) transfected with negative control, miR-490-3p mimics, miR-490-3p mimics plus TGFβR1. β-actin as loading control. e Representative images of wound healing assay and quantification carried out in negative control, miR-490-3p mimics or miR-490-3p mimics- plus TGFβR1-overexpressing ovarian cancer cells (SKOV3 and CaOV3) treated with 10 ng/ml TGFβ1. f Cell invasion assay and quantification showed invasiveness of negative control, miR-490-3p mimics or miR-490-3p mimics plus TGFβR1 overexpressing ovarian cancer cells (SKOV3 and CaOV3) treated with 10 ng/ml TGFβ1. g Westernblot analysis showed the protein level of EMT-associated markers (claudin, E-cadherin, N-cadherin, vimentin and MMP9) in negative control, miR-490-3p mimics or miR-490-3p mimics- plus TGFβR1-overexpressing ovarian cancer cells (SKOV3 and CaOV3). All cells were treated with 10 ng/ml TGFβ1. All data were represented as mean ± SD from three biological replicates (*P < 0.05; **P < 0.01)