Propofol modulates the proliferation, invasion and migration of bladder cancer cells through the miR-145-5p/TOP2A axis

Propofol-based anesthesia has been reported to reduce the recurrence and metastasis of a number of cancer types following surgical resection. However, the effects of propofol in bladder cancer (BC) are yet to be fully elucidated. The aim of the present study was to investigate the functions of propofol in BC and their underlying mechanisms. In the study, the expression of microRNA (miR)-145-5p in BC tissues and cell lines was evaluated using reverse transcription-quantitative PCR, and the effects of propofol on BC cells were determined using cell viability, wound healing and Transwell cell invasion assays, bioinformatics analysis, western blotting, immunohistochemistry and in vivo tumor xenograft models. It was found that propofol significantly suppressed the proliferation, migration and invasion of BC cells in vitro. In addition, propofol induced miR-145-5p expression in a time-dependent manner, and miR-145-5p knockdown attenuated the inhibitory effects of propofol on the proliferation, migration and invasion of BC cells. Topoisomerase II alpha (TOP2A) was a direct target of miR-145-5p, and silencing TOP2A reversed the effects of miR-145-5p knockdown in propofol-treated cells. Furthermore, propofol suppressed tumor xenograft growth, which was partially attenuated by miR-145-5p knockdown. The present study provided novel insight into the advantages of surgical intervention with propofol anesthesia in patients with BC.

Automated summary

Propofol has been found to significantly suppress the proliferation, migration, and invasion of bladder cancer cells in vitro, largely through the upregulation of miR-145-5p expression. Silencing the direct target of miR-145-5p, TOP2A, reversed the effects of propofol treatment in bladder cancer cells. Additionally, propofol was shown to suppress tumor xenograft growth, with partial attenuation by miR-145-5p knockdown.