Fig 1: CASK was one downstream target of miR-1245b-5p and boosted the progression of PCa. (A) Venn diagram exhibited the predicted target genes of miR-1245b-5p by the crosstalk of four databases (starbase, miRDB, targetscan and miRWalk), and 5 common genes were selected as the candidate genes. (B and C) qRT-PCR assays confirmed that the expression of CASK could be altered by the overexpression of miR-1245b-5p and silence of AATBC in PC3 and LNCAP cells. (D and E) The mRNA and protein expression of CASK was quantified in PCa cells and normal cells by qRT-PCR and Western blot, respectively. (F) RIP assay justified that AATBC, miR-1245b-5p and CASK could be coexisted in Ago2 pallets. (G) Bioinformatics database predicted the binding site between miR-1245b-5p and CASK. (H and I) Luciferase assay and RNA pull down assay elucidated the interaction between the miR-1245b-5p and CASK above the binding site. (J) The knockdown efficiency of miR-1245b-5p was validated by qRT-PCR. (K and L) CASK mRNA expression and protein levels were determined by RT-qPCR and Western blot in sh-NC, sh-AATBC and sh-AATBC+miR-1245b-5p inhibitors groups. (M) The knockdown competence of CASK was validated by qRT-PCR. (N–Q) The influence of biological function including colony formation (N), apoptosis (O), migration (P) and invasion (Q) were determined in PCa cells with the silence of CASKC. **P<0.01.