Abstract: Objective To investigate the expression of stimulator of interferon genes (STING) in patients with bladder cancer and its mechanism of regulating interferon- γ (IFN-γ)/signal transducer and activator of transcription 1 (STAT1) signaling pathway. 
Methods In this cohort study, 110 patients with bladder cancer were selected to collect cancer tissues and adjacent tissues, and the expression of STING in cancer tissues and adjacent tissues was detected by quantitative real-time polymerase chain reaction (qPCR). In cytological test, CRISPR-Cas9 technology was used to knock out the STING gene of human bladder cancer BIU-87 cells, and bladder cancer cells were divided into three groups: control group, NC group (transfected with NC plasmid) and experimental group (transfected with CRISPR-Cas9 plasmid). MTT method was used to detect the proliferation ability of cells at different time points (at 24 h, 48 h and 72 h), and flow cytometry was used to detect the proportion of cell survival, early apoptosis and late apoptosis in each group. qPCR was used to detect mRNA expression levels of IFN- γ and STAT1, and Western blot method for detecting IFN- γ and STAT1 protein expression level as well as the phosphorylation modification level of STAT1 protein. 
Results In cohort study, the expression level of STING in bladder cancer tissue was higher than that in adjacent tissue (P＜0.05). Cytological test showed that, compared with the control group, the proliferation ability of cells in the knockout STING group decreased, and further decreased with time (P＜0.05). Cell proliferation decreased cell survival, and the proportion of early and late apoptosis increased (P＜0.05). IFN- γ and STAT1 mRNA expression levels decreased (P＜0.05), and the expression level of IFN- γ and STAT1 protein as well as the phosphorylation level of STAT1 decreased (P＜0.05). 
Conclusion STING may activate the protein expression of IFN-γ/STAT1 signaling pathway and phosphorylation modification of STAT1, thereby getting involved in the occurrence and development of bladder cancer. 

Key words: urinary bladder neoplasms, stimulator of interferon genes, interferon-γ