Long non-coding RNA UCA1 promotes cell progression by acting as a competing endogenous RNA of ATF2 in prostate cancer.

Prostate cancer (PCa) is a leading cause of cancer-related deaths in elder men. This disease has limited therapeutic options and poor prognosis as the underlying molecular mechanisms are not clearly understood. LncRNA UCA1 functions as an oncogene in many types of cancers. However, the role of UCA1 in PCa remains unclear. In the present study, we showed that UCA1 was significantly up-regulated in PCa cell lines and tissue samples. High UCA1 expression was positively associated with high gleason score, advanced TNM stage and shorter overall survival of PCa patients. Inhibition of UCA1 suppressed PCa cells proliferation, migration and invasion in vitro. Moreover, UCA1 depletion inhibited the growth of PCa cells in vivo. In addition, we found that ATF2 was a direct target gene of UCA1. UCA1 regulated ATF2 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to ATF2 3'UTR, which suppressed the degradation of ATF2 mRNA by miR-204. In summary, we unveil a branch of the UCA1-miR-204-ATF2 pathway that regulates the progression of PCa. The inhibition of UCA1 expression may be a promising strategy for PCa therapy.