EIF 3 B silencing inhibits cell proliferation via regulating EGFR / ERK pathway in lung adenocarcinoma

Objective: We aimed to investigate the biological role of eukaryotic translation initiation factor 3B (EIF3B) and its mechanism in lung adenocarcinoma (LAD) occurrence. Methods: EIF3B was firstly determined in LAD tissues and cell lines using Western blot and quantitative real-time PCR. EIF3B was then knocked down using RNA interference technology in LAD cell lines, A549 and 95D. Furthermore, function analysis, including CCK-8, colony formation, cell cycle and apoptosis assay were conducted on A549 and 95D cells. Results: EIF3B protein was strongly upregulated in LAD samples compared to normal tissues. The same results were observed in lung cancer cell lines. Knockdown of EIF3B significantly inhibited the proliferation of LAD, induced cell cycle arrest and apoptosis. Furthermore, the proliferation inhibitory effect was associated with downregulation of p-EGFR and p-ERK induced by EIF3B silencing. Conclusion: These data suggest that EIF3B contributes to the proliferation of LAD cells might through regulating EGFR/ERK pathway.