UCA1 promotes cell viability, proliferation and migration potential through UCA1/miR-204/CCND2 pathway in primary cystitis glandularis cells.

Cystitis glandularis (CG) is an unusual proliferative disorder of the urinary bladder. Increasing evidences demonstrated that long non-coding RNAs (lncRNAs) play important roles in a variety of cellular progresses. However, there are rarely reports about the role and underlying molecular mechanism of lncRNAs in CG. In this study, we firstly isolated the primary cells from the tissues of CG and adjacent normal tissues, and found that UCA1 was up-regulated in the primary CG cells (pCGs). Then, we showed that knock out of UCA1 reduced the cell viability, inhibited the cell proliferation and restrained the migration potential and overexpression of UCA1 promoted that in pCGs. Furthermore, we demonstrated that UCA1 played its role via sponging of the miR-204 in pCGs. In addition, we illustrated that miR-204 exerted its function via targeting CYCLIN D2 (CCND2) 3'UTR at mRNA level in pCGs. Ultimately, we revealed the role and regulation of UCA1/miR-204/CCND2 regulatory axis in pCGs. In summary, our study, for the first time, revealed the role and underlying mechanism of an lncRNA UCA1 in CG, providing a potential biomarker and therapeutic target for human CG.