Sorting nexin 9 expression and prognostic implications in lung adenocarcinoma: integrative bioinformatic and in vitro validation.

BACKGROUND: Sorting nexin 9 (SNX9) is involved in intracellular vesicle transport and signal transduction, and its abnormal expression is related to the occurrence and development of a variety of cancers. In lung adenocarcinoma (LUAD), the role and molecular mechanism of SNX9 remain unclear. This study combined bioinformatics analysis and in vitro validation to explore its expression characteristics in LUAD, its specific effects on tumor development, and its potential molecular mechanism and prognostic value. METHODS: In this study, the expression data and clinical information of SNX9 in LUAD were obtained from Tumor Immune Estimation Resource (TIMER) 2.0, The Cancer Genome Atlas (TCGA) and Human Protein Atlas (HPA) databases, and the relationship between SNX9 expression and prognosis was analyzed using TCGA database patient information and Kaplan-Meier plotter, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were used to reveal the mechanism of SNX9. Gene set enrichment analysis (GSEA) enrichment analysis highlighted the pathways and biological processes rich in gene sets in SNX9 high-expression samples, thereby providing insights into associated enrichment pathways. The effects of SNX9 on the proliferation, migration and invasion of LUAD cells were detected by Western blot and in vitro experiments. RESULTS: The results of this study showed that the expression level of SNX9 in LUAD tissues was significantly higher than that in normal lung epithelial cells, and its high expression was closely related to the increase in tumor grade and poor prognosis of patients. Functional enrichment analysis showed that SNX9-related genes were concentrated in epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) and cell adhesion processes in LUAD, suggesting that the increased expression of SNX9 is positively correlated with the enhanced invasion ability of LUAD cells. In vitro experiments also showed that knockdown of endogenous SNX9 significantly inhibited the proliferation, migration and invasion of A549 and H1299 cells. CONCLUSIONS: This study shows that SNX9 is overexpressed in LUAD and is associated with poor prognosis. We speculate that SNX9 is expected to be a prognostic marker and a potential therapeutic target for LUAD, providing a new direction and theoretical basis for related research and clinical application.