MiR-200c inhibited the proliferation of oral squamous cell carcinoma cells by targeting Akt pathway and its downstream Glut1.

OBJECTIVE: Our study aimed to investigate the functionality of miR-200c in oral squamous cell carcinoma. METHODS: Tumor tissues and adjacent tissues were obtained from oral squamous cell carcinoma patients, and blood samples were extracted from both oral squamous cell carcinoma patients and healthy controls. Expression of miR-200c in those tissues was detected by qRT-PCR. All patients were followed-up for 5 years and ROC curves as well as survival analyses were performed to evaluate the diagnostic as well as prognostic values of serum miR-200c for oral squamous cell carcinoma. miR-200c and Glut1 overexpression oral squamous cell carcinoma cell lines were constructed and cell proliferation was detected by CCK-8 assay. Glucose uptake was determined by glucose uptake assay. Interactions between miR-200c, Akt and Glut1 were explored by western blot. RESULTS: Expression of miR-200c was significantly downregulated in tumor tissues comparing with adjacent tissues in most oral squamous cell carcinoma patients. Serum level of miR-200c was lower in oral squamous cell carcinoma patients than that in healthy controls, and it was decreased with increased primary tumor stages. Serum levels of miR-200c can been used to effectively distinguish oral squamous cell carcinoma patients from healthy control, and patients with lower serum level of miR-200c showed shorter survival time. miR-200c overexpression inactivated Akt and Glut1 expression, while Akt activator and Glut1 overexpression showed no significant effects on miR-200c. Akt activator promoted Glut1 expression, but Glut1 overexpression showed no significant effects on Akt. MiR-200c inhibited cell proliferation and glucose uptake, while Akt activator and Glut1 overexpression reduced the inhibitory effect of miR-200c overexpression on cell proliferation. CONCLUSION: miR-200c can inhibit the proliferation of oral squamous cell carcinoma cells by targeting Akt pathway and its downstream Glut1.