Wang Jin-Feng, Wang Jian-She, Liu Yang, Ji Bo, Ding Bei-Chen, Wang Ya-Xuan, Ren Ming-Hua
Department of Urology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Department of Urology, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, China.
Biofactors. 2025 Jan-Feb;51(1):e2150. doi: 10.1002/biof.2150. Epub 2024 Dec 7.
Bladder cancer (BC) is the most common urinary tract malignancy. Identifying biomarkers that predict prognosis and immune function in patients with BC can enhance our understanding of its pathogenesis and provide valuable guidance for diagnosis and treatment. Our findings indicate that increased ITGB1 expression is associated with higher clinical grade and stage, establishing ITGB1 as an independent prognostic risk factor for BC. Enrichment analysis revealed that the function of ITGB1 in BC was linked to the extracellular matrix. The experimental results showed that ITGB1 knockdown in the BC cell lines 5637 and RT112 reduced their proliferation, migration, and invasion. Furthermore, ITGB1 suppression promotes apoptosis in BC cells by inhibiting the PI3K-AKT pathway. A prognostic risk model incorporating CES1, NTNG1, SETBP1, and AIFM3 was developed based on ITGB1, this model can accurately predict patient prognosis based on immunological status. In conclusion, this study shows that knockdown of ITGB1 can restrain the migratory and invasive capabilities of BC cells and accelerate apoptosis, and this role might be associated with PI3K-AKT, highlighting its potential as a diagnostic marker and therapeutic target for BC.
膀胱癌（BC）是最常见的泌尿系统恶性肿瘤。识别可预测BC患者预后和免疫功能的生物标志物，能够增进我们对其发病机制的理解，并为诊断和治疗提供有价值的指导。我们的研究结果表明，整合素β1（ITGB1）表达增加与更高的临床分级和分期相关，确立了ITGB1作为BC的独立预后风险因素。富集分析显示，ITGB1在BC中的功能与细胞外基质相关。实验结果表明，在BC细胞系5637和RT112中敲低ITGB1可降低其增殖、迁移和侵袭能力。此外，抑制ITGB1通过抑制PI3K-AKT途径促进BC细胞凋亡。基于ITGB1建立了一个包含羧酸酯酶1（CES1）、神经纤毛蛋白1（NTNG1）、SET结合蛋白1（SETBP1）和凋亡诱导因子线粒体相关3（AIFM3）的预后风险模型，该模型可根据免疫状态准确预测患者预后。总之，本研究表明敲低ITGB1可抑制BC细胞的迁移和侵袭能力并加速凋亡，且这一作用可能与PI3K-AKT相关，凸显了其作为BC诊断标志物和治疗靶点的潜力。
