Fig. 4

PRMT5 is a direct target gene of the tumor suppressor miR-331-3p. A Schematic illustration of PRMT5 3’-UTR wild-type (WT) and miR-331-3p binding site mutated (Mut) PRMT5 3’-UTR luciferases reporter vectors. B Relative luciferase activities were measured in PC-3 and DU145 cells transfected with PRMT5 3’-UTR WT or Mut luciferases reporter vectors and miR-331-3p or NC mimics. C Relative luciferase activities were measured in PC-3 and DU145 cells transfected with PRMT5 3’-UTR WT or Mut luciferases reporter vectors and miR-331-3p inhibitor or NC mimics. D PRMT5 protein expression was detected by Western blot in PC-3 and DU145 cells transfected with miR-331-3p or NC mimics. E PRMT5 protein expression was detected by Western blot in PC-3 and DU145 cells transfected with miR-331-3p inhibitor or NC mimics. F Relative expression of miR-331-3p levels in PCa tumor and paired adjacent normal tissues (n = 248) by qRT-PCR. G and H Comparison of miR-331-3p levels in different Gleason scores (GS) and T stages were analyzed in PCa samples (n = 248). I Kaplan–Meier curve was used to evaluate the progression-free survival (PFS) of PCa patients with high (n = 124) or low (n = 124) miR-331-3p expression (Log-rank, P < 0.0001). J The correlation analysis between the expression levels of miR-331-3p and PRMT5 in our own patient cohort (n = 248; r = -0.5344, P < 0.01)