Bioinformatics Analysis Identified the Key Genes of Aspirin and Redox Damaged Yeast Cells
Bioinformatics Analysis Identified the Key Genes of Aspirin and Redox Damaged Yeast Cells
Hui-Ying Chen1,2*, Ping-Chuan Yin1,2, Ya-Nan Lu1,2, Hai-Yun Li1,2*and Yang Shan3
ABSTRACT
Aspirin is a widely used anti-inflammatory and antithrombotic drug that exhibits chemopreventive anti-tumor properties. Aspirin is considered to be partially mediated by the induction of apoptosis in cells. However, the underlying molecular mechanisms of aspirin in the prevention of cancer are yet to be fully elucidated. In the current study, the GSE115660 microarray dataset was downloaded from the Gene Expression Omnibus database to identify key genes in aspirin-damaged yeast cells following redox injury. Differentially expressed genes (DEGs) were subsequently identified and functionally enriched for analysis. Additionally, a protein-protein interaction network (PPI) was constructed and block analysis was performed using STRING and Cytoscape databases. A total of 248 genes were identified, of which 84 were downregulated and 164 were upregulated. Functional and pathway enrichment analyses indicated that upregulated genes were significantly involved in pyrimidine metabolism, glyoxylic acid metabolism and dicarboxylic acid metabolism. Downregulated genes were primarily implicated in secondary metabolite biosynthesis, carbon metabolism and antibiotic effects. The results revealed that the substance exhibited abundant biosynthesis and glycolysis/gluconeogenesis. Subsequently, the following top 10 hub genes were identified to the PPI network: Guanine nucleotide-binding protein subunit β, ribosomal 60S subunit protein (RPL) 8A, RPL9A, RPL6B, ribosomal 40S subunit protein (RPS) 9B, RPL31B, RPL27B, RPS14B, RPL22B and RPL22A. In conclusion, the DEGs and Hub genes identified in the present study may further elucidate the molecular mechanisms of aspirin applied to redox-damaged yeast cells and may identify potential future biomarkers.
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October 2020
Vol. 52, Iss. 5, Pages 1631-2026
