OBJECTIVE: To elucidate whether lncSNHG14 could influence the proliferative potential and cell cycle progression of bladder cancer cells via binding to microRNA-150-5p (miRNA-150-5p). We aim to investigate the potential mechanism of miRNA-150-5p in the occurrence and progression of bladder cancer (BCa). PATIENTS AND METHODS: Expression levels of SNHG14 and miRNA-150-5p in BCa tissues and normal bladder tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Their expressions in BCa cell lines were detected as well. Regulatory effects of NHG14 and miRNA-150-5p on proliferative potential and cell cycle progression were evaluated by cell counting kit-8 (CCK-8) and flow cytometry, respectively. Through the dual-luciferase reporter gene assay, binding conditions between SNHG14 and miRNA-150-5p, as well as between miRNA-150-5p and synaptic vesicle-associated membrane protein 2 (VAMP2), were verified. Finally, rescue experiments were performed to clarify whether SNHG14 regulated behaviors of BCa cells by absorbing miRNA-150-5p to degrade VAMP2. RESULTS: SNHG14 was highly expressed in BCa tissues and cell lines. The overexpression of SNHG14 accelerated the proliferative potential and cell cycle progression of BCa cells. SNHG14 was confirmed to bind to miRNA-150-5p. MiRNA-150-5p remained a low expression in BCa tissues. Moreover, miRNA-150-5p overexpression suppressed proliferative potential and cell cycle progression of BCa cells, which could reverse the promotive role of SNHG14 on behaviors of BCa cells. Furthermore, VAMP2 was the target gene of miRNA-150-5p. VAMP2 overexpression reversed the biological function of miRNA-150-5p in inhibiting proliferative potential and cell cycle progression of T24 and UC9 cells. CONCLUSIONS: LncSNHG14 overexpression accelerates proliferative potential and cell cycle progression of BCa cells through absorbing miRNA-150-5p to degrade VAMP2 expression.
OBJECTIVE: To elucidate whether lncSNHG14 could influence the proliferative potential and cell cycle progression of bladder cancer cells via binding to microRNA-150-5p (miRNA-150-5p). We aim to investigate the potential mechanism of miRNA-150-5p in the occurrence and progression of bladder cancer (BCa). PATIENTS AND METHODS: Expression levels of SNHG14 and miRNA-150-5p in BCa tissues and normal bladder tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Their expressions in BCa cell lines were detected as well. Regulatory effects of NHG14 and miRNA-150-5p on proliferative potential and cell cycle progression were evaluated by cell counting kit-8 (CCK-8) and flow cytometry, respectively. Through the dual-luciferase reporter gene assay, binding conditions between SNHG14 and miRNA-150-5p, as well as between miRNA-150-5p and synaptic vesicle-associated membrane protein 2 (VAMP2), were verified. Finally, rescue experiments were performed to clarify whether SNHG14 regulated behaviors of BCa cells by absorbing miRNA-150-5p to degrade VAMP2. RESULTS:SNHG14 was highly expressed in BCa tissues and cell lines. The overexpression of SNHG14 accelerated the proliferative potential and cell cycle progression of BCa cells. SNHG14 was confirmed to bind to miRNA-150-5p. MiRNA-150-5p remained a low expression in BCa tissues. Moreover, miRNA-150-5p overexpression suppressed proliferative potential and cell cycle progression of BCa cells, which could reverse the promotive role of SNHG14 on behaviors of BCa cells. Furthermore, VAMP2 was the target gene of miRNA-150-5p. VAMP2 overexpression reversed the biological function of miRNA-150-5p in inhibiting proliferative potential and cell cycle progression of T24 and UC9 cells. CONCLUSIONS: LncSNHG14 overexpression accelerates proliferative potential and cell cycle progression of BCa cells through absorbing miRNA-150-5p to degrade VAMP2 expression.