Abstract
A long noncoding RNA called SNHG17 (small nucleolar RNA host gene 17) is aberrantly expressed and plays essential roles in multiple human cancer types. Nevertheless, its expression pattern and specific functions in tongue squamous cell carcinoma (TSCC) have not been well studied until now. Hence, in this study, we aimed to measure SNHG17 expression in TSCC and to examine the actions of SNHG17 on the malignant characteristics of TSCC cells. The regulatory mechanism that mediates the oncogenic effects of SNHG17 on TSCC cells was investigated too. In this study, SNHG17 was found to be upregulated in TSCC, and this overexpression closely correlated with adverse clinical parameters and shorter overall survival among the patients with TSCC. The SNHG17 knockdown significantly decreased TSCC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Mechanism investigation revealed that SNHG17 acts as a competing endogenous RNA on microRNA-876 (miR-876) in TSCC cells. In addition, specificity protein 1 (SP1) was validated as a direct target gene of miR-876 in TSCC cells. SP1 expression restoration in TSCC cells reversed miR-876 overexpression-induced anticancer effects. MiR-876 downregulation strongly attenuated the actions of the SNHG17 knockdown in TSCC cells. SNHG17 plays an oncogenic part in TSCC cells both in vitro and in vivo via sponging of miR-876 and thereby upregulating SP1, which could be regarded as a promising target for TSCC therapy.