Zhang Daiyang, Liu Shiqing
Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, 430060, China.
J BUON. 2017 Jan-Feb;22(1):258-264.
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.
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.
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.
SOX5 is a novel regulator of EMT in OS, and is a potential target for OS.
SOX5在多种癌症中发挥重要作用。然而，SOX5在骨肉瘤（OS）中的表达及作用尚未得到充分研究。在本研究中，我们旨在探究SOX5在OS中的作用机制。
从骨肉瘤患者获取OS及相邻非癌组织标本。应用PCR检测SOX5 mRNA。随后对人骨肉瘤细胞系（U2OS、SoSP-M、SoSP-9607和MG-63）及一种永生化正常成骨细胞hFOB1.19进行研究。在U2OS中应用shRNA敲低SOX5，在MG-63中应用重组质粒上调SOX5。使用实时细胞监测系统和侵袭实验，并进行蛋白质印迹分析以检测E-钙黏蛋白、N-钙黏蛋白、波形蛋白和Snail的蛋白水平，以甘油醛-3-磷酸脱氢酶（GAPDH）作为对照。P<0.05被认为具有统计学意义。
在OS组织和细胞系中鉴定出SOX5显著上调。功能获得和功能丧失研究表明，SOX5显著促进OS细胞迁移和侵袭。此外，SOX5通过调节Snail促进上皮-间质转化（EMT）。
SOX5是OS中EMT的新型调节因子，是骨肉瘤的潜在治疗靶点。
