STIL enhances the development of lung adenocarcinoma by regulating the glycolysis pathway

作     者：Lei Wang Xianjin Xie 

作者机构：Department of Respiratory Medicine Jen Ching Memorial Hospital Suzhou 215300 China. Department of Respiratory Medicine Shandong Provincial Third Hospital Jinan 250010 China. 

出 版 物：《Oncology research》 (肿瘤学研究（英文）)

年 卷 期：2025年第33卷第1期

页      面：123-132页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：E2 promoter binding factor 1 Glycolysis Lung adenocarcinoma SCL/TAL1 interrupting locus (STIL) 

摘      要：Background:To investigate SCL/TAL 1 interrupting locus () s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined and E2 promoter binding factor 1 (E2F1) expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA). Methods:Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, and flow cytometry, elucidated and E2F1 s effects on cell viability, proliferation, apoptosis, and migration. Gene set enrichment analysis (GSEA) identified potential pathways, while metabolic assays assessed glucose metabolism. Results:Our findings reveal that and E2F1 are overexpressed in LUAD, correlating with adverse outcomes. It enhances cell proliferation, migration, and invasion, and suppresses apoptosis, activating downstream of E2F1. Silencing E2F1 reversed the promotion effect of the overexpression on cell viability and invasiveness. Importantly, modulates glycolysis, influencing glucose consumption, lactate production, and energy balance in LUAD cells. Conclusion:Our model, incorporating , age, and disease stage, robustly predicts patient prognosis, underscored s pivotal role in LUAD pathogenesis through metabolic reprogramming. This comprehensive approach not only confirms s prognostic value but also highlights its potential as a therapeutic target in LUAD.