Research and reports in urology · 2025
Influencing Factors and Risk Prediction Model Construction of Urinary Tract Infections in Patients with Bladder Cancer.
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Di Yancheng, Zhang Lingling, Zhao Linlin, Yin Lei
Аннотация
PURPOSE: Urinary tract infections (UTI) are a common complication in patients with bladder cancer (BLCA). This study investigated the role of stearoyl-CoA desaturase-1 (SCD1) in BLCA progression and assessed its potential as a biomarker for predicting UTI risk in BLCA patients.
PATIENTS AND METHODS: SCD1 expression profiles were evaluated in BLCA patients with concurrent UTI. Receiver operating characteristic curve analysis was used to assess the diagnostic value of SCD1 for predicting UTI risk. In vitro assays were conducted to explore the functional role of SCD1 in lipopolysaccharide (LPS)-associated BLCA progression.
RESULTS: SCD1 expression was significantly higher in the UTI group compared with the non-UTI group (p = 0.000 and 0.011, respectively). The combination of SCD1, immune-inflammation index, and C-reactive protein demonstrated strong predictive value for UTI risk in BLCA patients (non-muscle invasive BLCA patients: area under the curve (AUC) = 0.887; 95% CI: 0.821-0.935; muscle-invasive BLCA patients: AUC = 0.861; 95% CI: 0.767-0.927). Functional experiments revealed that lipopolysaccharide (LPS)-induced SCD1 expression promoted autophagy and enhanced malignant phenotypes, whereas SCD1 inhibition or treatment with an autophagosome inhibitor reversed these effects.
CONCLUSION: SCD1 promotes LPS-associated BLCA progression by regulating autophagy and may serve as a valuable biomarker for predicting UTI risk in BLCA patients.
PATIENTS AND METHODS: SCD1 expression profiles were evaluated in BLCA patients with concurrent UTI. Receiver operating characteristic curve analysis was used to assess the diagnostic value of SCD1 for predicting UTI risk. In vitro assays were conducted to explore the functional role of SCD1 in lipopolysaccharide (LPS)-associated BLCA progression.
RESULTS: SCD1 expression was significantly higher in the UTI group compared with the non-UTI group (p = 0.000 and 0.011, respectively). The combination of SCD1, immune-inflammation index, and C-reactive protein demonstrated strong predictive value for UTI risk in BLCA patients (non-muscle invasive BLCA patients: area under the curve (AUC) = 0.887; 95% CI: 0.821-0.935; muscle-invasive BLCA patients: AUC = 0.861; 95% CI: 0.767-0.927). Functional experiments revealed that lipopolysaccharide (LPS)-induced SCD1 expression promoted autophagy and enhanced malignant phenotypes, whereas SCD1 inhibition or treatment with an autophagosome inhibitor reversed these effects.
CONCLUSION: SCD1 promotes LPS-associated BLCA progression by regulating autophagy and may serve as a valuable biomarker for predicting UTI risk in BLCA patients.