Background: Ameloblastomas are odontogenic neoplasms characterized by local invasiveness. This study was conducted to address the role of matrix metalloproteinase-2 (MMP-2) in the invasiveness of ameloblastomas. Methods: Plasmids containing either MMP-2 siRNA or tissue inhibitor of metalloproteinase-2 (TIMP-2) cDNA were created and subsequently transfected into primary ameloblastoma cells. Zymography, RT-PCR, and Western blots were used to assess MMP-2 activity and expression of MMP-2 and TIMP-2, as well as protein levels. Results: Primary cultures of ameloblastoma cells expressed cytokeratin (CK) 14 and 16, and MMP-2, but only weakly expressed CK18 and vimentin. MMP-2 mRNA and protein levels were significantly inhibited by RNA interference (P < 0.05). Both MMP-2 siRNA and TIMP-2 overexpression inhibited MMP-2 activity and the in vitro invasiveness of ameloblastoma. Conclusion: These results indicate that inhibition of MMP-2 activity suppresses the local invasiveness of ameloblastoma cells. This mechanism may serve as a novel therapeutic target in ameloblastomas pursuant to additional research.

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.