Epigenetic silencing of miRNA is a primary mechanism of aberrant miRNA 
expression in cancer, and hypermethylation of miRNA promoters has been reported 
to contribute to prostate cancer initiation and progression. Recent data have 
shown that the miR-193b promoter is hypermethylated in prostate cancer compared 
with normal tissue, but studies assessing its functional significance have not 
been performed. We aimed to elucidate the function of miR-193b and identify its 
critical targets in prostate cancer. We observed an inverse correlation between 
miR-193b level and methylation of its promoter in The Cancer Genome Atlas (TCGA) 
cohort. Overexpression of miR-193b in prostate cancer cell lines inhibited 
invasion and induced apoptosis. We found that a majority of the top 150 genes 
downregulated when miR-193b was overexpressed in liposarcoma are overexpressed 
in metastatic prostate cancer and that 41 miR-193b target genes overlapped with 
the 86 genes in the aggressive prostate cancer subtype 1 (PCS1) signature. 
Overexpression of miR-193b led to the inhibition of the majority of the 41 genes 
in prostate cancer cell lines. High expression of the 41 genes was correlated 
with recurrence of prostate cancer. Knockdown of miR-193b targets FOXM1 and RRM2 
in prostate cancer cells phenocopied overexpression of miR-193b. Dual treatment 
with DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors 
decreased miR-193b promoter methylation and restored inhibition of FOXM1 and 
RRM2. Our data suggest that silencing of miR-193b through promoter methylation 
may release the inhibition of PCS1 genes, contributing to prostate cancer 
progression and suggesting a possible therapeutic strategy for aggressive 
prostate cancer.