Objective: Osteosarcoma is the second highest cause of cancer-related death in children, mainly due to development of often fatal metastasis, usually in the lungs. Glucocorticoids play an important role in the treatment of a number of inflammatory diseases and immune diseases. The objective of this study was to explore the molecular mechanism of osteosarcoma in response to dexamethasone (DEX, a kind of synthetic glucocorticoid), with a view to obtain information on the pathways activated by DEX.
Materials and methods: By using the GSE6711 Affymetrix microarray data accessible from Gene Expression Omnibus database, we first identified the differentially expressed genes (DEGs) among different time course treatment with dexamethasone of each isoform, and the DEGs among cells expressing different GR isoforms, followed by the pathway enrichment analysis of the DEGs.
Results: The results indicated that DEX could inhibit osteosarcoma cell proliferation and promote osteosarcoma cell apoptosis through induction of lots of related genes expression at the transcription level.
Conclusions: Our data provide a comprehensive bioinformatics analysis of pathways which may be involved in the response to glucocorticoids.