The transcribed-ultraconserved regions (T-UCRs) are a novel class of non-coding 
RNAs, which are absolutely conserved (100%) between the orthologous regions of 
the human, rat and mouse genomes. Previous studies have described that several 
T-UCRs show differential expressions in cancers and might be involved in cancer 
development. We investigated the transcriptional levels of representative 26 
T-UCRs and determined the regions that were differently expressed in prostate 
cancer (PCa) and gastric cancer (GC). A quantitative reverse 
transcription-polymerase chain reaction analysis revealed the downregulation of 
Uc.158+A expression by a DNA methylation-associated mechanism, which was 
restored by 5-Aza-dC (5-aza-2'-deoxycytidine) treatment. Bisulfite genomic 
sequencing using cell lines and tissue samples demonstrated cancer-specific CpG 
hypermethylation in both GC and PCa. However, Uc.416+A was only overexpressed in 
GC and we identified an miR-153 binding site in the possible regulatory region 
of Uc.416+A using online databases. Along with a forced expression or knockdown 
of miR-153 in MKN-74 GC cells, the transcriptional levels of Uc.416+A were 
significantly disturbed. A luciferase reporter gene assay supported the direct 
regulation of Uc.416+A expression by miR-153. Furthermore, Uc.416+A was 
associated with cell growth through the regulation of IGFBP6 (insulin-like 
growth factor-binding protein 6) in GC. These findings suggest an oncogenic role 
of Uc.416+A in GC, which suggests that our approach would provide new insights 
into functional studies of T-UCRs in cancer biology.