TY  - EJOU
AU  - WANG, LEI 
AU  - XIE, XIANJIN 

TI  - <i>STIL</i> enhances the development of lung adenocarcinoma by regulating the glycolysis pathway
T2  - Oncology Research

PY  - 2025
VL  - 33
IS  - 1
SN  - 1555-3906

AB  -  <b>Background:</b> To investigate SCL/TAL 1 interrupting locus (<i>STIL</i>)’s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined <i>STIL</i> and E2 promoter binding factor 1 (E2F1) expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA). <b>Methods:</b> Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, and flow cytometry, elucidated <i>STIL</i> 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. <b>Results:</b> Our findings reveal that <i>STIL</i> 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 <i>STIL</i> overexpression on cell viability and invasiveness. Importantly, <i>STIL</i> modulates glycolysis, influencing glucose consumption, lactate production, and energy balance in LUAD cells. <b>Conclusion:</b> Our model, incorporating <i>STIL</i>, age, and disease stage, robustly predicts patient prognosis, underscored <i>STIL</i>’s pivotal role in LUAD pathogenesis through metabolic reprogramming. This comprehensive approach not only confirms <i>STIL</i>’s prognostic value but also highlights its potential as a therapeutic target in LUAD.
KW  - SCL/TAL1 interrupting locus (<i>STIL</i>); Lung adenocarcinoma; E2 promoter binding factor 1; Glycolysis

DO  - 10.32604/or.2024.048562