Identification of potential target genes associated with the effect of propranolol on angiosarcoma via microarray analysis.

Abstract

The purpose of the present study was to explore the effect of propranolol on angiosarcoma, and the potential target genes involved in the processes of proliferation and differentiation of angiosarcoma tumor cells. The mRNA expression profile (GSE42534) was downloaded from the Gene Expressed Omnibus database, including three samples without propranolol treatment (control), three samples with propranolol treatment for 4 h and three samples with propranolol treatment for 24 h. The differentially expressed genes (DEGs) in angiosarcoma tumor cells with or without propranolol treatment were obtained via the limma package of R and designated DEGs-4 h and DEGs-24 h. The DEGs-24 h group was divided into two sets. Set 1 contained the DEGs also contained in the DEGs-4 h group. Set 2 contained the remainder of the DEGs. Functional and pathway enrichment analysis of sets 1 and 2 was performed. The protein-protein interaction (PPI) networks of sets 1 and 2 were constructed, termed PPI 1 and PPI 2, and visualized using Cytoscape software. Modules of the two PPI networks were analyzed, and their topological structures were simulated using the tYNA platform. A total of 543 and 2,025 DEGs were identified in angiosarcoma tumor cells treated with propranolol for 4 and 24 h, respectively, compared with the control group. A total of 401 DEGs were involved in DEGs-4 h and DEGs-24 h, including metallothionein 1, heme oxygenase 1, WW domain-binding protein 2 and sequestosome 1. Certain significantly enriched gene ontology (GO) terms and pathways of sets 1 and 2 were identified, containing 28 overlapping GO terms. Furthermore, 121 nodes and 700 associated pairs were involved in PPI 1, whereas 1,324 nodes and 11,839 associated pairs were involved in PPI 2. A total of 45 and 593 potential target genes were obtained according to the node degrees of PPI 1 and PPI 2. The results of the present study indicated that a number of potential target genes, including AXL receptor tyrosine kinase, coatomer subunit α, DR1-associated protein 1 and ERBB receptor feedback inhibitor 1 may be involved in the effect of propranolol on angiosarcoma.