v>hsa-miR-195-5p (miR-195) has been proven to be acritical regulator in the progression of prostate cancer (PCa). Toidentify additional targets and molecular functions of miR-195,we overexpressed miR-195 by transient oligonucleotide transfection in DU145 and LNCaP cells and examined the effects.RNA-based microarray and dual-luciferase assays werecarried out to identify novel targets of miR-195, while in vitrofunctional assays, a subcutaneous xenograft model, tissuemicroarray (TMA) analysis and a cohort of publicly availabledata (Taylor cohort) were used to investigate the biologicalfunction and clinical value of miR-195 targeting. The resultsshown that miR-195 overexpression could markedly suppresscellular proliferation and tube formation compared withmiR-negative control. The RNA-based microarray identifieda total of 153 differentially regulated genes with fold changesof ≤|1.5|, including 138 (90.2%) downregulated and 15 (9.8%)upregulated genes. Among the downregulated genes, we foundthat proline-rich protein 11 (PRR11) combined with miR-195expression (miR-195/PRR11) could be used as an independentpredictor of the risk of biochemical recurrence in the Taylorcohort. Additionally, the dual-luciferase assay identifiedPRR11 as a novel target of miR-195, and the in vitro assaysindicated that PRR11 abrogated the suppressive effects ofmiR-195 on cell proliferation, tube formation and cell cycling.Furthermore, the subcutaneous tumor xenograft model indicated that knockdown of PRR11 inhibited xenograft growthand angiogenesis, while the results of the TMA and Taylorcohort analyses collectively demonstrated that PRR11 expression was upregulated in aggressive tumors and is associatedwith poor clinical outcome. Taken together, these findingsfurther illustrate the suppressive role of miR-195 in PCa, andindicate a novel role of PRR11 in PCa. Importantly, the newlyidentified miR-195/PRR11 axis may aid with identifyingpotential therapeutic targets in PCa.