Bioinformatic and experimental analyses of key biomarkers in pancreatic cancer

The present study aimed to screen the key genes in pancreatic cancer and to explore the pathogenesis of pancreatic cancer. A total of three expression profiling datasets (GSE28735, GSE16515 and GSE15471) associated with pancreatic cancer were retrieved from the public gene chip database. The differentially expressed genes (DEGs) were screened by GEO2R and subjected to Gene Ontology (GO) and signaling pathway enrichment analysis. Furthermore, a protein interaction network was constructed. The GEPIA online database was used to screen for genes that affect the prognosis of pancreatic cancer. Finally, cell functional experiments were performed on the selected key genes. A total of 72 DEGs were identified, including 52 upregulated and 20 downregulated genes. Enrichment analysis revealed roles of the DEGs in endodermal cell differentiation, cell adhesion, extracellular matrix-receptor interaction and PI3K-Akt signaling pathway. In total, 10 key nodal genes were identified, including integrin subunit alpha 2 (ITGA2), ITGB6 and collagen alpha 1 chain 1. Through survival analysis, two genes with an impact on the prognosis of pancreatic cancer were identified, namely ITGA2 and ITGB6. Silencing of ITGB6 in a pancreatic cancer cell line significantly suppressed cell proliferation and induced cell cycle arrest at G2/M phase. The identified key genes and signaling pathways may help to deepen the understanding of the molecular mechanisms involved in pancreatic cancer and provide a theoretical basis to develop novel therapies.

Automated summary

This study aimed to identify key genes in pancreatic cancer by analyzing gene expression profiling data. Through enrichment analysis, it was found that these genes were involved in important biological processes such as endodermal cell differentiation, cell adhesion, extracellular matrix-receptor interaction, and the PI3K-Akt signaling pathway. ITGA2 and ITGB6 were identified as key genes impacting the prognosis of pancreatic cancer, with experimental results showing that silencing ITGB6 can inhibit pancreatic cancer cell proliferation.