Open Access
ARTICLE
STIL enhances the development of lung adenocarcinoma by regulating the glycolysis pathway
LEI WANG1, XIANJIN XIE2,*
1 Department of Respiratory Medicine, Jen Ching Memorial Hospital, Suzhou, 215300, China
2 Department of Respiratory Medicine, Shandong Provincial Third Hospital, Jinan, 250010, China
* Corresponding Author: XIANJIN XIE. Email: 
Oncology Research https://doi.org/10.32604/or.2024.048562
Received 12 December 2023; Accepted 19 April 2024; Published online 29 May 2024
Abstract
Background: To investigate STIL centriolar assembly protein (STIL)’s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined STIL and E2 promoter binding factor 1 (E2F1) expressions 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. 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, underscoring 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.
Keywords
SCL/TAL1 interrupting locus (STIL); Lung adenocarcinoma; E2 promoter binding factor 1; Glycolysis
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