miR-101 Inhibits AKT/mTOR and Attenuates Oral Cancer Cell Colony Formation and Epithelial-Mesenchymal Transition

Epithelial mesenchymal transition (EMT) is a most effective way for tumors invasion and metastasis. Our study explored miR-101’s role in the formation and epithelial-mesenchymal transition of oral cancer cells. Cancer and adjacent tissues were removed from patients with clinical oral squamous cell carcinoma. Real-time quantitative PCR or immunoblotting was used to detect miR-101 and EMT-related indicators expression. In addition, miR-101 was overexpressed in oral cancer cell lines followed analysis of the effect of miR-101on cell colony formation and epithelial-mesenchymal transition. Luciferase reporter gene assay validated the target relationship between miR-101 and AKT. Compared with adjacent tissues, tumor tissues showed significantly decreased expression of miR-101 and E-cadherin and elevated N-cadherin. The N-cadherin level was related to the malignancy. After overexpression of miR-101, the ability of cell clone formation was weakened, the number of clone formation was decreased, the migration ability was significantly reduced, and cell EMT was inhibited. Luciferase reporter gene experiments showed that miR-101 has a targeting effect on AKT. miR-101 is up-regulated in oral cancer patients. In oral cancer cell lines, miR-101 overexpression can attenuate oral cancer cell colony formation and epithelial-mesenchymal transition by inhibiting AKT/mTOR, providing theoretical basis for targeted treatment of oral squamous cell carcinoma to reduce metastasis and recurrence and improve the cure rate of patients.