Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Department of Radiation and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Bioengineered. 2022 Apr;13(4):10180-10190. doi: 10.1080/21655979.2022.2061278.
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. 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 was also verified . 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-κB inhibitor. CTSV is upregulated and promotes proliferation through the NF-κB pathway in bladder cancer and may be a potential target in inflammation-associated bladder cancer.
慢性炎症与膀胱癌的发展呈正相关。然而，其详细的调节机制仍不清楚。采用实时定量聚合酶链反应（PCR）测量相对基因的 mRNA 水平。通过 Western blot 监测蛋白水平。通过细胞计数试剂盒 8（CCK8）和集落形成实验分别评估细胞增殖和活力。通过双荧光素酶报告基因检测评估转录活性。还在裸鼠中进行了实验。TCGA 数据库分析表明，组织蛋白酶 V（CTSV）的异常表达与膀胱癌患者的不良预后相关。CTSV 增强了炎症反应，促进了膀胱癌的发展。CTSV 的过表达增加了膀胱癌细胞的增殖和活力。相反，CTSV 的缺失显著抑制了膀胱癌细胞的增殖和活力。CTSV 缺乏导致的肿瘤抑制作用也得到了验证。此外，多种癌症相关的荧光素酶筛选表明，CTSV 的过表达触发了炎症信号通路，而 NF-κB 抑制剂可以恢复该信号通路。CTSV 在膀胱癌中通过 NF-κB 通路上调并促进增殖，可能是炎症相关膀胱癌的潜在靶点。
