miRNAs have proven to be key regulators of gene expression and are 
differentially expressed in various diseases, including cancer. Our aim was to 
identify epigenetically dysregulated genes in prostate cancer. We performed 
miRNA expression profiling after relieving epigenetic modifications in 6 
prostate cancer cell lines and nonmalignant prostate epithelial cells. 
Thirty-eight miRNAs showed increased expression in any prostate cancer cell line 
after 5-aza-2'-deoxycytidine (5azadC) and trichostatin A (TSA) treatments. Six 
of these also had decreased expression in clinical prostate cancer samples 
compared to benign prostatic hyperplasia. Among these, miR-193b was methylated 
in 22Rv1 cell line at a CpG island approximately 1 kb upstream of the miRNA 
locus. Expressing miR-193b in 22Rv1 cells using pre-miR-193b oligonucleotides 
caused a significant growth reduction (p < 0.001) resulting from a decrease of 
cells in S-phase of the cell cycle (p < 0.01). In addition, the anchorage 
independent growth was partially inhibited in transiently miR-193b-expressing 
22Rv1 cells (p < 0.01). Altogether, our data suggest that miR-193b is an 
epigenetically silenced putative tumor suppressor in prostate cancer.