D Xu1, M Gu, H-L Liu. 1. Department of Stomatology, The Third Affiliated Hospital of Soochow University, The First People's Hospital of Changzhou City, Changzhou, China. gumin106@163.com.
Abstract
OBJECTIVE: The aim of this study was to investigate the role of microRNA-625-3p in the occurrence and progression of oral squamous cell carcinoma (OSCC) and its underlying mechanism. PATIENTS AND METHODS: Expression levels of microRNA-625-3p, SCAI and E-cadherin in OSCC tissues and paracancerous tissues were detected by quantitative real time-polymerase chain reaction (qRT-PCR). MicroRNA-625-3p expression in OSCC tissues with different tumor stages and lymph node metastasis stages was analyzed. Survival analyses were conducted to access the diagnostic values of microRNA-625-3p and SCAI in OSCC. The effect of microRNA-625-3p on regulating cell migration of OSCC was detected by transwell assay. Luciferase reporter gene assay was conducted to verify the binding condition between microRNA-625-3p and SCAI. Rescue experiments were performed by co-transfection of microRNA-625-3p inhibitor and si-SCAI, followed by cell proliferation detection. RESULTS: MicroRNA-625-3p was highly expressed in OSCC tissues than that of paracancerous tissues. OSCC patients with T3+T4 presented higher expression of microRNA-625-3p than those with T1+T2. Similarly, OSCC patients with N1+N2 presented higher expression of microRNA-625-3p than those with N0. Luciferase reporter gene assay identified that SCAI is the target gene of microRNA-625-3p. Furthermore, we found that SCAI and E-cadherin are lowly expressed in OSCC tissues than that of paracancerous tissues. ROC curve showed that microRNA-625-3p and SCAI exert certain values in diagnosing OSCC. MicroRNA-625-3p promoted migration of OSCC cells, which was reversed by SCAI knockdown. CONCLUSIONS: MicroRNA-625-3p is highly expressed in OSCC, which promotes cell migration of OSCC by regulating SCAI expression.
OBJECTIVE: The aim of this study was to investigate the role of microRNA-625-3p in the occurrence and progression of oral squamous cell carcinoma (OSCC) and its underlying mechanism. PATIENTS AND METHODS: Expression levels of microRNA-625-3p, SCAI and E-cadherin in OSCC tissues and paracancerous tissues were detected by quantitative real time-polymerase chain reaction (qRT-PCR). MicroRNA-625-3p expression in OSCC tissues with different tumor stages and lymph node metastasis stages was analyzed. Survival analyses were conducted to access the diagnostic values of microRNA-625-3p and SCAI in OSCC. The effect of microRNA-625-3p on regulating cell migration of OSCC was detected by transwell assay. Luciferase reporter gene assay was conducted to verify the binding condition between microRNA-625-3p and SCAI. Rescue experiments were performed by co-transfection of microRNA-625-3p inhibitor and si-SCAI, followed by cell proliferation detection. RESULTS: MicroRNA-625-3p was highly expressed in OSCC tissues than that of paracancerous tissues. OSCC patients with T3+T4 presented higher expression of microRNA-625-3p than those with T1+T2. Similarly, OSCC patients with N1+N2 presented higher expression of microRNA-625-3p than those with N0. Luciferase reporter gene assay identified that SCAI is the target gene of microRNA-625-3p. Furthermore, we found that SCAI and E-cadherin are lowly expressed in OSCC tissues than that of paracancerous tissues. ROC curve showed that microRNA-625-3p and SCAI exert certain values in diagnosing OSCC. MicroRNA-625-3p promoted migration of OSCC cells, which was reversed by SCAI knockdown. CONCLUSIONS: MicroRNA-625-3p is highly expressed in OSCC, which promotes cell migration of OSCC by regulating SCAI expression.