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

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.