Accumulating　evidence　reports　that　Capn4　plays　an　important　role　in　the　development　and　progression　of　various　malignant　cancers.　However,　whether　Capn4　is　involved　in　prostate　cancer　remains　unclear.　Therefore,　the　aim　of　this　study　was　to　investigate　the　expression,　biological　function　and　regulatory　mechanism　of　Capn4　in　prostate　cancer.　Herein,　we　found　that　Capn4　was　highly　expressed　in　prostate　cancer　cell　lines　compared　with　normal　prostate　cells.　Capn4　gene　silencing　markedly　suppressed　the　growth,　invasion　and　Wnt/β-catenin　signaling　of　prostate　cancer　cells,　whereas　Capn4　overexpression　showed　an　oncogenic　effect.　Moreover,　silencing　of　β-catenin　significantly　blocked　the　oncogenic　effect　of　Capn4　overexpression.　Bioinformatics　analysis　predicted　that　Capn4　was　a　potential　target　gene　of　microRNA-520b　(miR-520b),　which　has　been　reported　as　a　tumor　suppressive　miRNA　in　various　cancers.　The　dual-luciferase　reporter　assay　confirmed　that　miR-520b　directly　bound　to　the　3＇-untranslated　region　of　Capn4.　Real-time　quantitative　PCR　and　Western　blot　analysis　showed　that　miR-520b　negatively　regulated　Capn4　expression　in　prostate　cancer　cells　in　vitro.　Furthermore,　we　found　that　miR-520b　was　significantly　downregulated　in　prostate　cancer　cell　lines　and　tissues.　In　addition,　miR-520b　expression　was　inversely　correlated　with　Capn4　expression　in　prostate　cancer　clinical　specimens.　Overexpression　of　miR-520b　mimicked　the　tumor　suppressive　effect　of　Capn4　siRNA,　whereas　inhibition　of　miR-520b　had　an　oncogenic　effect.　Restoration　of　Capn4　significantly　blocked　the　antitumor　effect　of　miR-520b　in　prostate　cancer　cells.　Overall,　our　findings　demonstrate　an　oncogenic　role　of　Capn4　in　prostate　cancer　and　show　that　its　expression　is　epigenetically　regulated　by　miR-520b.　Our　results　reveal　that　suppression　of　Capn4　by　miR-520b　inhibits　the　growth　and　invasion　of　prostate　cancer　cells　associated　with　downregulated　Wnt/β-catenin　signaling,　indicating　an　important　role　of　the　miR-520b/Capn4/Wnt/β-catenin　regulation　axis　in　the　molecular　pathogenesis　of　prostate　cancer.　Our　study　suggests　that　miR-520b　and　Capn4　may　represent　potential　and　novel　therapeutic　targets　for　prostate　cancer.