STAU1 exhibits oncogenic characteristics and modulates alternative splicing and gene expression in A549 lung adenocarcinoma cells

Staufen double-stranded RNA-binding protein 1 (STAU1) assumes a significant role in cancer development and is correlated with survival outcomes in patients with lung cancer. Nevertheless, its specific functions and molecular mechanisms in lung adenocarcinoma (LUAD) remain insufficiently explored. In our research, we established a STAU1 knockdown expression model within the A549 cell line. We discerned that the knockdown of STAU1 significantly suppressed the proliferation, invasion, and migration of A549 cells and enhanced the level of cell apoptosis. Through RNA-seq analysis, we identified 197 differentially expressed genes (DEGs) and 1,362 STAU1-Regulated alternative splicing Events (ASEs). The DEGs were specifically enriched in cell adhesion pathways, while the ASE genes were mainly associated with cell division and the cell cycle. Our study implies that STAU1 possesses oncogenic characteristics and may modulate DEGs and ASEs to affect the proliferation, invasion, and migration of A549 cells. This research provides novel insights that might contribute to the diagnosis and treatment of LUAD. We established a STAU1 knockdown model in the A549 cell line and integrated it with RNA-seq data to thoroughly disclose the biological functions of STAU1 in A549 cells and analyze the alterations in the transcriptome subsequent to STAU1 Knockdown.