miR-617 represses SERPINE1 production and reduces tumorigenic traits in oral squamous cell carcinoma cells
Background: Serpin family E member 1 (SERPINE1) is a serine proteinase inhibitor (serpin) upregulated in diverse types of cancer, including Oral squamous cell carcinoma (OSCC) and functions as an oncogenic role. Hence, exploring pathological mechanism underlying SERPINE1 high expression is crucial to the targeted therapy of OSCC. Methods: Bioinformatics analysis was performed to identify the miRNA and the candidate gene contributing to OSCC progression. The viability, proliferation and apoptosis of the OSCC cell were evaluated using CCK-8 assay, BrdU assay, and cell apoptosis assay, respectively. The RNA pull-down assay and luciferase reporter assay were conducted to verify the relationship between SERPINE1 and miR-617. Results: SERPINE1 was aberrantly upregulated in OSCC tissues and cell lines. Genetically inhibiting SERPINE1 led to reduction of OSCC cell viability and proliferation while elevation of OSCC cell apoptosis. By bioinformatics analysis, miR-617 contained a response element for SERPINE1 overexpression, which is validated by the RNA pull-down and luciferase reporter assay. Furthermore, miR-617 was detected to be downregulated in OSCC tissues and cell lines as well as displayed a negative correlation with advanced stage. Besides, miR-617 mimic or inhibitor transfection could suppress or boost the SERPINE1 expression. More importantly, miR-617 mimic could block the effect of SERPINE1 overexpression on OSCC cells proliferation, viability and apoptosis. Conclusion: SERPINE1 acted as a pro-proliferative oncogenic factor which is partly regulated by miR-167 downregualtion in OSCC cells. Therefore, miR-617/SERPINE1 axis is a potential therapeutic target against OSCC.