Comprehensive analysis of the oncogenic potential of eukaryotic initiation factor 3M via SAAL1 interaction in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) carries a poor prognosis at advanced stages underscoring the need to elucidate the underlying molecular mechanisms driving its pathogenesis. This study aimed to investigate the roles of eukaryotic translation initiation factor 3 subunit M () and its associated effector, serum amyloid A-like 1 (), in LUAD development and progression. Bioinformatic analyses such as TNMplot, The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and other public databases were used to evaluate and expression levels, methylation status, clinical associations, and potential transcriptional regulators across LUAD datasets. Patient samples were analyzed for / expression by qRT-PCR, immunohistochemistry, and ELISA. and were overexpressed in LUAD tumor tissues compared with normal lung tissues, correlated with advanced stage, nodal metastasis, and poor survival outcomes. High / levels associated with increased cell proliferation, epithelial-mesenchymal transition, metastasis, and regulatory T cell dysfunction based on gene set enrichment analysis (GSEA). Mechanistically, / upregulation was linked to promoter hypomethylation, and transcriptionally regulated by JMJD1C, via hTFtarget prediction. The / promote oncogenic cellular programs and immunosuppressive microenvironments that conferred unfavorable prognosis. These findings nominate EIF3M/SAAL1 as potential therapeutic targets and biomarkers in LUAD.