SOX5 promotes epithelial-mesenchymal transition in osteosarcoma via regulation of Snail.

PURPOSE: SOX5 plays important roles in various kinds of cancers. However, the expression and roles of SOX5 in osteosarcoma (OS) have not been investigated well. In the present study we aimed to investigate the mechanism of SOX5 in OS.

METHODS: OS and adjacent non-cancerous specimens were obtained from patients with OS. PCR was applied to detect SOX5 mRNA. Then human OS cell lines (U2OS, SoSP-M, SoSP-9607, and MG-63) and one immortalized normal osteoblast hFOB1.19 were investigated. SOX5 knocking with shRNA in U2OS and SOX5 upregulation with recombinant plasmid in MG-63 were applied. Real-time cell monitoring system and invasion assay were used, and Western blot assay was performed to detect the protein level of E-cadherin, N-cadherin, Vimentin and Snail, where Glyceraldehyde3- phosphate dehydrogenase (GAPDH) was presented as control. P<0.05 was considered as statistically significant.

RESULTS: Significant upregulation of SOX5 in OS tissues and cell lines was identified. The gain- and loss-of-function studies suggested that OS cell migration and invasion were promoted significantly by SOX5. Additionally, SOX5 promoted epithelial-mesenchymal transition (EMT) by regulation of Snail.

CONCLUSION: SOX5 is a novel regulator of EMT in OS, and is a potential target for OS.