Identification of hub genes, key pathways, and therapeutic agents in Hutchinson-Gilford Progeria syndrome using bioinformatics analysis.

摘要: Background Hutchinson-Gilford Progeria syndrome (HGPS) is a rare lethal premature and accelerated aging disease caused by mutations in the lamin A/C gene. Nevertheless, mechanisms of cellular damage, senescence, HGPS are not fully understood. Therefore, we aimed to screen potential key genes, pathways, therapeutic agents using bioinformatics methods this study. Methods The gene expression profile GSE113648 GSE41751 were retrieved from omnibus database analyzed identify differentially expressed genes (DEGs) between normal controls. Then, ontology Kyoto encyclopedia genomes pathway enrichment analysis carried out. To construct protein-protein interaction (PPI) network, used STRING Cytoscape make module these DEGs. Besides, connectivity map (cMAP) tool was as well predict drugs. Results As result, 180 upregulated DEGs 345 downregulated identified, which significantly enriched pathways cancer PI3K-Akt signaling pathway. top centrality hub fibroblast growth factor 2, decorin, matrix metallopeptidase2, Fos proto-oncogene, AP-1 transcription subunit screened out critical among PPI network. Dexibuprofen parthenolide predicted be possible for treatment cMAP analysis. Conclusion This study identified signal agents, might help us improve our understanding some new HGPS.