Downregulation of BLM RecQ helicase inhibits proliferation, promotes the apoptosis and enhances the sensitivity of bladder cancer cells to cisplatin.

Bloom syndrome protein (BLM) is known to maintain genomic integrity including DNA repair, recombination, replication and transcription. Its dysregulation affects the genomic instability of cells, which results in a high risk of developing various types of cancer and even Bloom syndrome. However, to date, to the best of our knowledge, no association has been made between human BLM and bladder cancer. Thus, the aim of the present study was to investigate the role of BLM in human bladder cancer. The expression pattern of BLM in bladder cancer tissue was detected by immunohistochemistry. The viability, proliferation, cell cycle and apoptosis of bladder cancer cell lines were determined by Cell Counting Kit‑8, EdU and flow cytometry following transfection of BLM small interfering RNA. Finally, the effect of BLM on sensitivity of bladder cancer cell lines to cisplatin was investigated by reverse transcription‑quantitative PCR and western blot. It was demonstrated that the expression of BLM in human bladder cancer was increased compared with adjacent healthy bladder tissues. In addition, silencing of BLM inhibited the proliferation and promoted the apoptosis of bladder cancer cells and it also enhanced the sensitivity of bladder cancer cells to cisplatin. Together, the findings of the present study demonstrated that the regulation of BLM activity may have potential for use as a novel therapeutic target and a predictor for the prognosis of bladder cancer.