miR-222 knockdown suppresses epithelial-to-mesenchymal transitionin human oral squamous cell carcinoma.

Tumor metastasis is the main cause of death in patients with oral squamous cell carcinoma (OSCC). Epithelial-to-mesenchymal transition (EMT) is potentially associated with metastasis and histological grading in OSCC. Therefore, the discovery of new strategies to inhibit EMT is potentially valuable for the development of therapies for OSCC. In our previous study, we found that miR-222, which is up-regulated in OSCC, regulates the biological behavior of OSCC cells by targeting the p53-upregulated modulator of apoptosis (PUMA); however, the effect of miR-222 on TGF-β1-induced EMT in OSCC cells is unclear. In this study, OSCC cell lines CAL-27 and Tca-8113 were incubated with 5 ng/ml of TGF-β1 to inhibit the expression of E-cadherin, promote the expression of N-cadherin, vimentin, and α-SMA and stimulate achange in cell shape convert from a "cuboidal" epithelial structure into an elongated mesenchymal shape. We found that the expression of miR-222 was up-regulated during TGF-β1-induced EMT in OSCC cells. In addition, miR-222 knockdown reversed TGF-β1-induced EMT by targeting PUMA. Our findings indicate that miR-222 plays an important role in OSCC, potentially serving as a novel therapeutic target for the treatment of OSCC.