Abstract
Tongue squamous cell carcinoma (TSCC) is highly malignant and poorly differentiated, resulting in a high frequency of local recurrence and distant metastases. Sox2 (Sry‑box2), an important factor in embryonic development and cell differentiation, has been shown to associate with malignant phenotypes and epithelial‑mesenchymal transition (EMT) progression in numerous types of human tumors. However, the clinical relevance and molecular mechanisms of Sox2 in TSCC remain unclear. In the present study, the expression levels of Sox2 were assessed in 61 pairs of TSCC samples and corresponding adjacent non-cancerous tissues using immunohistochemical methods. Associations between Sox2 expression and clinicopathological features were evaluated. Furthermore, Sox2 was overexpressed and inhibited using full-length Sox2 cDNA and short hairpin RNA (shRNA) transfection in UM2 and Cal27 cell lines, respectively. The malignant phenotypes were assessed by plate clone formation assays, wound-healing assays and Transwell assays. EMT markers (E‑cadherin, vimentin, Twist, Slug and Snail) and β‑catenin were detected by reverse transcription‑polymerase chain reaction and western blot analysis following the alterations of Sox2 expression. The results indicated that Sox2 expression was markedly upregulated in TSCC samples and was significantly associated with tumor growth (pT stage), cell differentiation, lymphatic metastasis (pN stage) and clinical stage (pTNM stage). Cal27‑shRNA‑Sox2 cells not only exhibited a decreased capacity for cell proliferation, but also suppressed cell migration and invasion, and an attenuated colony formation capacity. By contrast, UM2‑Sox2 cells exhibited accelerated cell malignant phenotypes and EMT progression. Moreover, when the expression of Sox2 was decreased by shRNA transduction, β‑catenin expression was attenuated. An opposing phenomenon was observed in UM2‑Sox2 cells. In conclusion, this study suggests that Sox2 expression serves a role in TSCC malignant phenotypes and EMT progression, and that β‑catenin may act as a modulated factor in this progression.