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The current study aimed to evaluate the possible role of microRNA (miR)-202 in the development of oral cancer. First, miR-202 levels were found to be decreased in the serum and tissues of oral cancer patients compared with healthy controls. Receiver operating characteristic analysis was carried out to explore the diagnostic value of serum miR-202 for oral cancer. Overexpression of miR-202 significantly decreased the migratory capacity of SCC-9 cells, while inhibition of miR-202 markedly increased the migratory capacity of SCC-9 cells. Moreover, the invasive capacity was decreased in SCC-9 cells transfected with an miR-202 mimic. In addition, the invasive capacity was enhanced in SCC-9 cells transfected with an miR-202 inhibitor. A dual luciferase reporter assay showed that overexpression of miR-202 markedly suppressed the relative luciferase activity of the pmirGLO-SP1-3'untranslated region. Overexpression of miR-202 suppressed the protein level of Sp1, but inhibition of miR-202 markedly enhanced the protein expression of Sp1. Inhibition of miR-202 enhanced the phosphorylation of protein kinase B. Additionally, the correlations between the expression levels of Sp1 and miR-202 and the clinicopathological factors of oral cancer were analyzed. The results showed that patients with high expression of Sp1 and miR-202 progressed to earlier clinical stages, had deeper infiltration depths and were more prone to lymph node metastasis compared with the healthy controls. In conclusion, the current study presented novel data indicating that decreased miR-202 enhanced the progression of oral cancer via Sp1.

Reduced miR‑202 levels enhanced oral cancer development via targeting Sp1