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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: The putative tumour suppressor miR-1-3p modulates prostate cancer cell aggressiveness by repressing E2F5 and PFTK1

Fig. 3

E2F5 and PFTK-1 were identified as direct target genes of miR-1-3p and down-regulated by miR-1-3p in the prostate cancer cell. a and b Schematic diagram of the predicted target binding sites of miR-1-3p in the 3′-UTR of E2F5 and PFTK-1. The seed recognition site is denoted. All nucleotides of the 3′-UTR region of E2F5 and PFTK-1 that binds with miR-1-3p are highly conserved across species as predicated by TargetScan (http://www.targetscan.org/vert_72/). c and d The luciferase activity of the wild type E2F5/ PFTK-1 3’-UTR (Wt) and mutant E2F5/ PFTK-1 3’-UTR (Mut) co-transfected with miR-1-3p mimics or a miRNA negative control (miR-LacZ) was measured in LnCap cells. Relative luciferase activity was plotted as the mean ± S.D. of three independent experiments. e-g Expression of PFTK-1 and E2F5 mRNA in LnCap, 22RV1 and RWPE-1 cells were assessed by RT-qPCR following transfection with miR-1-3p mimics, miR-1-3p inhibitor, or their negative controls (NC). GAPDH served as a loading control. h and i Western blot analysis of the protein levels and relative expression of E2F5 and PFTK-1 in response to 100 nM of indicated RNAs molecules. GAPDH served as a loading control in LnCap and 22RV1 cells. (*P < 0.05, **P < 0.01)

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