Fig. 5

miR-186-5p inhibits migration, invasion and EMT by targeting PIK3R3 in EOC cells. a Venn diagram showing the 33 putative miR-186-5p target genes which were significantly up-regulated in the mRNA arrays and predicted to be a target of miR-186-5p. b Schema showing the cloning of wild type as well as a mutant PIK3R3 3’UTR in which the two putative miR-186-5p binding sites were mutated in a luciferase reporter construct. c Direct interaction of miR-186-5p and PIK3R3 3’UTR on the putative miR-186-5p binding sites as shown by the specific reduction of relative luciferase reporter activities in cells co-transfected with miR-186-5p and wild type PIK3R3 #UTR reporter construct. d PIK3R3 expression was suppressed in EOC cells transfected siRNA against PIK3R3 and this could be partly rescued by the co-transfection of miR-186-5p inhibitors, as shown in RT-qPCR with GAPDH normalization. e EOC cells transfected with si-PIK3R3 showed reduced ability to migrate and invade in vitro as measured through wound healing and trans-well assays (imaged at × 200 magnification) than control cells, with a corresponding increase in E-cadherin (an epithelial marker) and decrease in Vimentin (a mesenchymal marker) as well as Twist and Rac1 levels. These changes in phenotypes could be partially rescued with the co-transfection of miR-186-5p inhibitors which partially rescued PIK3R3 expression (quantitation graph of WB refer to Additional file 3: Figure S2D/E). f, g Relative wound healing rate (f) and transwell migration/invasion(g) from at least three independent experiments as described in(E). h Relative expression of HOXD-AS1, miR-186-5p, PIK3R3, Twist and Rac1 in EOC cells transfected with siRNA against HOXD-AS1 or si-NC control