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

Abstract

Background: To investigate SCL/TAL 1 interrupting locus (STIL)'s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined STIL 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 STIL 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 STIL 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 STIL overexpression on cell viability and invasiveness. Importantly, STIL modulates glycolysis, influencing glucose consumption, lactate production, and energy balance in LUAD cells.

Conclusion: Our model, incorporating STIL, age, and disease stage, robustly predicts patient prognosis, underscored STIL's pivotal role in LUAD pathogenesis through metabolic reprogramming. This comprehensive approach not only confirms STIL's prognostic value but also highlights its potential as a therapeutic target in LUAD.