EIF3B regulates the cell cycle of lung adenocarcinoma cells by activating the GTSE1 mediated ERK/MAPK pathway.

OBJECTIVE: To preliminary explore the expression pattern, clinical significance, and potential molecular mechanism of EIF3B in lung adenocarcinoma (LUAD), and to provide preliminary evidence for its potential as a diagnostic and prognostic biomarker and therapeutic target (to be further verified by subsequent experiments). METHODS: LUAD data were obtained from multiple databases, and various statistical methods were used to analyze the correlation between EIF3B expression and clinical characteristics as well as prognosis. Cell experiments (transfection, wound healing, etc.), mouse subcutaneous tumor models, and Western blotting were combined to explore the function and mechanism of EIF3B. RESULTS: EIF3B was highly expressed in LUAD tissues, which was associated with advanced staging and poor prognosis, with a diagnostic AUC value of 0.911. Knockdown of EIF3B inhibited the proliferation and migration of cancer cells, while overexpression promoted these processes. EIF3B activated the ERK/MAPK pathway by positively regulating GTSE1, thereby regulating cell cycle proteins. In mouse experiments, knockdown of EIF3B reduced tumor volume by approximately 60% and tumor weight by approximately 55% without affecting health. CONCLUSION: EIF3B drives LUAD progression through the “EIF3B-GTSE1-ERK/MAPK-cell cycle” axis and has dual potential as a diagnostic and therapeutic target. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12931-026-03559-9.