SOX10 induces epithelial-mesenchymal transition and contributes to nasopharyngeal carcinoma progression.

OBJECTIVE: The aim of this study was to investigate the role of SOX10 in NPC and the underlying molecular mechanisms. METHODS: Expression of SOX10 was initially assessed in human NPC tissues and a series of NPC cell lines through quantitative real-time PCR (qRT-PCR) and western blot. Then, cell proliferation, cycle, migration and invasion of NPC cells with knockdown of SOX10 were examined by MTT, flow cytometry, transwell migration and invasion assay, respectively. Finally, nude mice tumorigenicity experiments were performed to evaluate the effects of SOX10 on NPC growth and metastasis in vivo. RESULTS: SOX10 was significantly increased in NPC tissues and cell lines. In vitro experiments revealed that loss of SOX10 obviously inhibited cell proliferation, migration and invasion, as well as epithelial-mesenchymal transition (EMT) process in NPC cells. In vivo experiments further demonstrated that disrupted SOX10 expression restrained NPC growth and metastasis, especially in lung and liver. CONCLUSION: Taken together, our data confirmed the role of SOX10 as an oncogene in NPC progression, and revealed that SOX10 may serve as a novel biomarker for diagnosis of NPC, as well as a potential therapeutic target against this disease.