W Xia1, C Chen, M-R Zhang, L-N Zhu. 1. Department of Urinary Surgery, the First People's Hospital of Changzhou, Changzhou, China. linazhu@fphcz.com.
Abstract
OBJECTIVE: Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in tumorigenesis of bladder cancer (BC). Our research aimed to explore the underlying mechanisms of lncRNA prostate cancer-associated transcript 6 (PCAT6) in BC. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain reaction (RT-qPCR) was used to measure the levels of PCAT6 and miR-513a in BC tissues and cells. The Kaplan-Meier analysis was utilized to evaluate the overall survival time of BC patients. Besides, cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were evaluated by wound healing and transwell assays. Furthermore, starBase and Dual-Luciferase reporter assay were used to determine the interaction between PCAT6 and miR-513a in BC cells. RESULTS: PCAT6 expression was upregulated, while miR-513a was downregulated in BC tissues and cell lines. BC patients with high expression of PCAT6 exhibited a shorter overall survival time compared with those patients with low expression of PCAT6. Moreover, PCAT6 knockdown notably suppressed cell progression. In addition, PCAT6 inhibited miR-513a expression through direct interaction, and the silencing of PCAT6 remarkably increased the expression of miR-513a. Finally, the knockdown of miR-513a partly abolished PCAT6 silencing-induced inhibitory effects on BC progression. CONCLUSIONS: Our study illustrated that PCAT6 knockdown inhibited cell progression of BC by regulating miR-513a, suggesting that PCAT6 might act as a prognostic biomarker and therapeutic target for BC patients.
OBJECTIVE: Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in tumorigenesis of bladder cancer (BC). Our research aimed to explore the underlying mechanisms of lncRNA prostate cancer-associated transcript 6 (PCAT6) in BC. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain reaction (RT-qPCR) was used to measure the levels of PCAT6 and miR-513a in BC tissues and cells. The Kaplan-Meier analysis was utilized to evaluate the overall survival time of BC patients. Besides, cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were evaluated by wound healing and transwell assays. Furthermore, starBase and Dual-Luciferase reporter assay were used to determine the interaction between PCAT6 and miR-513a in BC cells. RESULTS:PCAT6 expression was upregulated, while miR-513a was downregulated in BC tissues and cell lines. BC patients with high expression of PCAT6 exhibited a shorter overall survival time compared with those patients with low expression of PCAT6. Moreover, PCAT6 knockdown notably suppressed cell progression. In addition, PCAT6 inhibited miR-513a expression through direct interaction, and the silencing of PCAT6 remarkably increased the expression of miR-513a. Finally, the knockdown of miR-513a partly abolished PCAT6 silencing-induced inhibitory effects on BC progression. CONCLUSIONS: Our study illustrated that PCAT6 knockdown inhibited cell progression of BC by regulating miR-513a, suggesting that PCAT6 might act as a prognostic biomarker and therapeutic target for BC patients.