Long non-coding RNA TTN-AS1 promotes cell proliferation and inhibits cell apoptosis in prostatic cancer by sponging miR-193a-5p.

Abstract

Prostatic cancer (PCa) is a common cancer in males. Long non-coding RNA (lncRNA) TTN-AS1 has been reported as an oncogene in diverse cancers. This study aimed to explore the functions and mechanism of TTN-AS1 in PCa. The levels of TTN-AS1 and miR-193a-5p in PCa cells (DU145, PC3, 22RV1, C4-2B, and LNCaP) were measured by qRT-PCR. The putative target of TTN-AS1 was predicted by starBase v2.0 online database, and this interaction was validated by Dual-Luciferase reporter assay. The cell viability and apoptosis rate in DU145 and PC3 cells were assessed by MTT assay and flow cytometry, respectively. The protein levels of CyclinD1, p21, p27, Bcl-2, Bax, and cleaved-caspase3 were detected by Western blot. The relative expression of TTN-AS1 was apparently up-regulated, and the level of miR-193a-5p was strikingly down-regulated in PCa cells. The interaction between TTN-AS1 and miR-193a-5p was predicted by starBase v2.0 online database and verified by Dual-Luciferase reporter assay. The functional experiments indicated that TTN-ASI knockdown or miR-193a-5p inhibited cell viability and induced cell apoptosis rate in DU145 and PC3 cells. Furthermore, the recuperated experiments exhibited that miR-193a-5p inhibitor counteracted the inhibitory effect on cell viability and the promotion effect on cell apoptosis rate in DU145 and PC3 cells induced by TTN-AS1 silencing. These data indicated that TTN-AS1 was dramatically up-regulated, and miR-193a-5p was significantly down-regulated in PCa cells. The functional and mechanistical experiments unraveled that lncRNA TTN-AS1 sponged miR-193a-5p to promote cell proliferation and repress cell apoptosis in prostatic cancer, and this new regulatory pathway may shed light on the mechanism of prostatic cancer.