CTSV (cathepsin V) promotes bladder cancer progression by increasing NF-κB activity

Chronic inflammation is positively associated with the development of urinary bladder cancer. However, its detailed regulatory mechanism remains elusive. The quantitative real-time polymerase chain reaction was used to measure mRNA levels of relative genes. The protein levels were monitored by western blotting. Cell proliferation and viability were evaluated by the cell counting Kit 8 (CCK8) and colony formation assays, respectively. The dual-luciferase reporter assay was performed to assay the transcriptional activity. In vivo experiments were implemented in nude mice as well. The TCGA database analysis suggested that the aberrant expression of cathepsin V (CTSV) was related to a poor outcome in bladder cancer patients. CTSV boosted the inflammation reaction, which facilitated the development of bladder cancer. The overexpression of CTSV increased the proliferation and viability of bladder cancer cells. On the contrary, the deletion of CTSV significantly inhibited the proliferation and viability of bladder cancer cells. The tumor repression resulting from CTSV deficiency in vitro was also verified in vivo. Moreover, multiple cancer-associated luciferase screening showed that the overexpression of CTSV triggered the inflammatory signaling pathway, which could be restored by introducing the NF-kappa B inhibitor. CTSV is upregulated and promotes proliferation through the NF-kappa B pathway in bladder cancer and may be a potential target in inflammation-associated bladder cancer. [GRAPHICS] .

Automated summary

This study reveals that the aberrant expression of cathepsin V (CTSV) is associated with a poor outcome in bladder cancer patients. CTSV enhances the inflammatory reaction, thereby promoting the development of bladder cancer. Overexpression of CTSV increases the proliferation and viability of bladder cancer cells, while deletion of CTSV significantly inhibits their proliferation and viability. Furthermore, overexpression of CTSV activates the inflammatory signaling pathway, which can be restored by introducing an NF-kappa B inhibitor.