Expression and clinical significance of centromere protein A in pancreatic cancer based on GEO and TCGA database analysis / 中华胰腺病杂志

ABSTRACT

Objective:To study the expression and clinical value of centromere protein A (CENP-A) in pancreatic cancer (PC), and to predict the role of CENP-A in the development and progression of PC.Methods:The expression profile of CENP-A mRNA and clinicopathological data were obtained from PC data set downloaded from the gene expression omnibus (GEO) and the cancer genome atlas (TCGA), which included a microarray data set of 45 patients with PC (GSE28735) and a microarray data set of 177 patients with PC. The correlation between CENP-A gene expression in PC tissue and the clinicopathological indices as well as the effects on the prognosis of PC was analyzed by the bioinformatics method. The potential pathway regulated by CENP-A in PC was predicted by gene set enrichment analysis (GSEA). Meanwhile, the proteins related to CENP-A were screened out by combining with the protein-protein interaction (PPI) network of CENP-A in STRING database, and the correlation between CENP-A and expression of its related proteins was analyzed.Results:The expression level of CENP-A mRNA in PC tissue was greatly higher than that in adjacent tissue, and the difference was statistically significant (4.492±0.361 vs 3.431±0.405, P=0.001). The expression level of CENP-A in PC tissue was significantly correlated with TNM stage and tumor grade ( P<0.05). The overall survival of patients with high CENP-A expression was significantly lower than that of patients with low CENP-A expression ( P<0.05). Cell cycle and DNA replication pathways were enriched in PC tissue with high CENP-A expression ( P<0.01, false discovery rate<0.05). CENP-A in PC tissue was strongly correlated with CDK1 ( r=0.861, P<0.001) and BUB1 ( r=0.825, P<0.001) in PC tissue through the PPI network analysis. Conclusions:CENP-A gene overexpression in PC tissue was related to its malignant biological behaviour, and its mechanism may be achieved by the synergistic action with CDK1 and BUB1.