MicroRNA‑663b Downregulation Inhibits Proliferation and Induces Apoptosis in Bladder Cancer Cells by Targeting TUSC2

The present study aimed to explore the role and underlying molecular mechanism of microRNA‑663b (miR‑663b) in the tumorigenesis of bladder cancer. The miR‑663b expression in human bladder cancer tissues and cell lines was measured determined reverse transcription‑quantitative polymerase chain reaction. TargetScan was used to predict the potential targets of miR‑663b, and a dual‑luciferase reporter assay was performed to validate tumor suppressor candidate 2 (TUSC2) as a target of miR‑663b. Cell Counting Kit‑8 was used for cell viability analysis, and cell apoptosis was evaluated by flow cytometry. In addition, western blot analysis was performed to detect protein expression in current study. The findings suggested that miR‑663b was upregulated in bladder cancer tissues and cell lines compared with normal tissue and cells. TUSC2 was validated as a direct target of miR‑663b and was negatively regulated by miR‑663b. miR‑663b inhibition significantly reduced the viability of T24 cells, and T24 cell apoptosis was markedly induced. In addition, miR‑663b inhibition enhanced the expression levels of p53 and p21 in T24 cells. Furthermore, the changes caused by miR‑663b inhibitor in T24 cells were eliminated by TUSC2 gene silencing. In conclusion, inhibition of miR‑663b reduced viability and induced apoptosis in bladder cancer cells by targeting TUSC2. These findings provide a promising novel therapeutic target for bladder cancer treatment.