Abstract
BackgroundOral squamous cell carcinoma (OSCC) is one of the most common malignancies and has a poor prognosis. The epithelial-to-mesenchymal transition (EMT) is crucial for increasing the metastasis of OSCC. Recently, studies have indicated that sirtuin7 (SIRT7) is implicated in tumor genesis; however, the potential role of SIRT7 in the EMT and metastasis of OSCC has not been reported.MethodsWe investigated the cellular responses to SIRT7 silencing or overexpression in OSCC cell lines by wound healing assay, migration and invasion assay, western blotting, immunofluorescence and immunohistochemistry.ResultsIn the present study, we found that SIRT7 was significantly downregulated in OSCC cell lines and human OSCC/OSCC tissues with lymph node metastasis. Overexpression of SIRT7 decreased the proliferation and invasion of OSCC cells in vitro, whereas SIRT7 knockdown significantly increased OSCC cell growth and invasion. Upregulation of SIRT7 concomitantly increased the expression of E-cadherin, and decreased the expression of mesenchymal markers. SIRT7 overexpression also reduced the level of acetylated SMAD4 in OSCC cells. Moreover, SIRT7 overexpression significantly inhibited OSCC lung metastasis in vivo.ConclusionTogether, these findings suggested that SIRT7 suppressed EMT in OSCC metastasis by promoting SMAD4 deacetylation.
Highlights
Oral squamous cell carcinoma (OSCC) is one of the most common malignancies and has a poor prognosis
SIRT7 expression is correlated with OSCC progression We first determined whether SIRT7 expression was associated with human OSCC progression
The results showed that there was a significantly lower level of SIRT7 expression in P and M tissues than in NC tissues, which was confirmed by Western blot (WB) analysis (Fig. 1c–d)
Summary
Oral squamous cell carcinoma (OSCC) is one of the most common malignancies and has a poor prognosis. The epithelial-to-mesenchymal transition (EMT) is crucial for increasing the metastasis of OSCC. Oral cancer is one of the most common life-threatening types of cancer worldwide, with oral squamous cell carcinoma (OSCC) being the predominant form, accounting for over 90% of all oral malignancies [1,2,3,4]. The epithelial-to-mesenchymal transition (EMT) is a vital and fundamental process in the progression and metastasis of OSCC [3, 11,12,13,14]. Activation of the EMT results in decreased expression of epithelial markers (E-cadherin and β-catenin) and increased expression of adhesion and mesenchymal proteins (including vimentin, N-cadherin and fibronectin) [16, 17]. Transforming growth factor-β (TGF-β) signaling is a key regulator of EMT, which is
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