Kinesin family member 23 (KIF23) contributes to the progression of bladder cancer cells in vitro and in vivo

The aim of our study was to detect the expression of KIF23 in human bladder cancer tissues and to assess the potential role of KIF23 in bladder cancer progression. The expression of KIF23 and the correlation with bladder cancer patients were explored using the TCGA database. Additionally, IHC assays were also performed to detect KIF23 expression in 95 bladder cancer tissues and corresponding non-twnor tissues collected in our hospital. Colony formation, MTT, and flow cytometry (FCM) assays were performed to detect its effects on bladder cancer cell proliferation and apoptosis, respectively. An animal model was developed to found the effects of KIF23 on tumor growth in mice. Data showed that the KIF23 expression was upregulated in human bladder cancer tissues. The expression of KIF23 was correlated with the prognosis and clinicopathological features, including T stage (p=0.022) and recurrence (p=0.020), of bladder cancer patients. KIF23 depletion inhibited the proliferation of bladder cancer cells, stimulated apoptosis, and suppressed tumor growth in mice. We demonstrated the involvement of KIF23 in bladder cancer progression and provided a promising therapeutic target for the treatment of bladder cancer.

Automated summary

This study showed that KIF23 expression was upregulated in human bladder cancer tissues and correlated with the prognosis and clinicopathological features of patients. Depletion of KIF23 inhibited bladder cancer cell proliferation, induced apoptosis, and suppressed tumor growth in mice, suggesting a potential therapeutic target for bladder cancer treatment.