Aurora kinase A (AURKA) promotes the progression and imatinib resistance of advanced gastrointestinal stromal tumors

Abstract Background Gastrointestinal stromal tumor (GIST) is a common that originates from the alimentary system mesenchyme. Compared to typical gastrointestinal carcinomas, GISTs exhibit unique malignant behaviors. Bioinformatic tools and subsequent experiments were applied investigate novel targets involved in GIST progression imatinib resistance. Methods Differences gene expression profiles between advanced nonadvanced comprehensively analyzed based on Gene Expression Omnibus (GEO) dataset GSE136755. A protein–protein interaction (PPI) network was constructed identify potential target gene. set enrichment analysis (GSEA) used elucidate relevant biological events related GSE47911 dataset. Subsequently, immunohistochemistry Kaplan–Meier performed validate prognostic value of GISTs. Overexpression conducted analyze its function proliferation, apoptosis, resistance GIST/T1 cells. Results In current study, total 606 differentially expressed genes (DEGs) screened GSE136755 dataset, upregulated DEGs mainly cell division through functional annotations. The intersecting hub gene, Aurora kinase (AURKA), identified by degree bottleneck algorithms. GSEA revealed AURKA cycle-related processes. Analysis Oncomine GEPIA databases pattern elevated most human malignances. Clinical assays demonstrated could be an independent factor for Additionally, overexpression experimentally promote inhibit enhance Conclusions These findings indicated promoted enhanced resistance, implying therapeutic