Analysis of the molecular mechanism of osteosarcoma using a bioinformatics approach.

The aim of this study was to explore the underlying molecular mechanism related to the process and progression of osteosarcoma (OS). The differentially expressed genes (DEGs) were downloaded from the Gene Expression Omnibus database. The pathway and gene ontology (GO) enrichment analysis, as well as transcription factor, tumor-associated gene and tumor suppressor gene analyses were performed to investigate the functions of DEGs. Next, the protein-protein interaction (PPI) network was constructed and module analysis was further assessed by cluster analysis with the overlapping neighborhood expansion (Cluster ONE) cytoscape plug-in. A total of 359 upregulated and 614 downregulated DEGs were identified to be differentially expressed between OS samples and normal controls. Pathways significantly enriched by DEGs included the focal adhesion and chromosome maintenance pathways. Significant GO terms were cell adhesion, cell cycle and nucleic acid metabolic processes. The upregulated PPI network was constructed with 170 nodes and the downregulated PPI network was constructed with 332 nodes. Breast-ovarian cancer gene 1 (BRCA1), melanocyte-stimulating hormone 2 (MSH2), cyclin D1 (CCND1) and integrin α5 (ITGA5) were identified to be hub proteins in PPI. In conclusion, the dysregulated genes played key roles in the progression of OS. Cell adhesion is a significant biological process in OS development, and the genes BRCA1, MSH2, CCND1 and ITGA5 may be potential targets in the therapy of OS.