BACKGROUND: MicroRNAs are noncoding small RNA that negatively regulate target gene expression by binding to the 3'-UTR of mRNA. Previous studies have shown that several microRNAs play a pivotal role in prostate cancer by acting as oncogenes or tumor suppressors. This study was aimed at identifying microRNAs that contribute to the progression to castration resistant prostate cancer. METHODS: MicroRNAs expression profiles of a xenograft model and cell lines were examined by microarray analysis and real-time PCR. Functional analysis of miR-582-5p in cellular proliferation was examined by cell counting. Furthermore, in order to investigate a candidate target of miR-582-5p, microarray analysis and analysis in silico were utilized. RESULTS: MiR-582-5p was identified to be up-regulated at the castration resistant stage of a xenograft model, KUCaP2 and in castration resistant cell line, AILNCaP#1. Overexpression of miR-582-5p increased the number and the percentage of S phase of LNCaP cells under androgen deprived condition. Moreover, suppression of miR-582-5p decreased the number and the percentage of S phase of AILNCaP#1 cells. Furthermore, we identified that miR-582-5p down-regulates EFNB2 expression, which is down-regulated at the castration resistant stage of a xenograft model, KUCaP2 and in castration resistant cell line, AILNCaP#1. CONCLUSIONS: Our results suggest that up-regulation of miR-582-5p contributes to an increase in the proliferation of prostate cancer cells under androgen deprived conditions.
BACKGROUND: MicroRNAs are noncoding small RNA that negatively regulate target gene expression by binding to the 3'-UTR of mRNA. Previous studies have shown that several microRNAs play a pivotal role in prostate cancer by acting as oncogenes or tumor suppressors. This study was aimed at identifying microRNAs that contribute to the progression to castration resistant prostate cancer. METHODS: MicroRNAs expression profiles of a xenograft model and cell lines were examined by microarray analysis and real-time PCR. Functional analysis of miR-582-5p in cellular proliferation was examined by cell counting. Furthermore, in order to investigate a candidate target of miR-582-5p, microarray analysis and analysis in silico were utilized. RESULTS:MiR-582-5p was identified to be up-regulated at the castration resistant stage of a xenograft model, KUCaP2 and in castration resistant cell line, AILNCaP#1. Overexpression of miR-582-5p increased the number and the percentage of S phase of LNCaP cells under androgen deprived condition. Moreover, suppression of miR-582-5p decreased the number and the percentage of S phase of AILNCaP#1 cells. Furthermore, we identified that miR-582-5p down-regulates EFNB2 expression, which is down-regulated at the castration resistant stage of a xenograft model, KUCaP2 and in castration resistant cell line, AILNCaP#1. CONCLUSIONS: Our results suggest that up-regulation of miR-582-5p contributes to an increase in the proliferation of prostate cancer cells under androgen deprived conditions.