CircRNA_002178 promotes the proliferation and migration of oral squamous cell carcinoma cells by activating the Akt/mTOR pathway.

Abstract

We aimed to investigate the biological effects of circRNA_002178 in oral squamous cell carcinoma (OSCC) tissues and to analyze its potential mechanism. CircRNA_002178 expression in 50 pairs of OSCC tissues and adjacent ones was studied by quantitative polymerase chain reaction (qPCR) analysis, and the correlations of circRNA_002178 with clinicopathological indicators, as wells as prognosis of OSCC patients were analyzed. qPCR was used to verify circRNA_002178 expression in OSCC cell lines. Subsequently, circRNA_002178 knockdown models were constructed using lentivirus in OSCC cell lines, and the impacts of circRNA_002178 on the function of OSCC cells were assessed by cell counting kit-8 (CCK-8) test, plate cloning experiment, transwell assay and nude mouse tumor formation experiments. Finally, rescue experiments in vitro were used to explore the potential mechanism of circRNA_002178 activating Akt/mTOR pathway. Our data showed that circRNA_002178 expression in OSCC tissue specimens was remarkably higher than that in adjacent ones. In comparison to patients in low circRNA_002178 expression group, patients in high expression group showed higher incidences of advanced pathological stage and distant metastasis, and a lower overall survival rate. Cell functional experiments revealed that knockdown of circRNA_002178 markedly attenuated the proliferation and migration ability of OSCC cells compared to the sh-NC group, and the consistent results were observed in the nude mouse experiment. In addition, Western blot suggested that the expression of key proteins in Akt/mTOR signaling pathway was remarkably reduced after downregulation of circRNA_002178 in OSCC cells. Meanwhile, Akt activator SC79 reversed the inhibitory effect of circRNA_002178 on the metastasis and proliferation of OSCC cells. CircRNA_002178, over-expressed in OSCC tissues and cell lines, may promote the malignant progression of OSCC through activating the Akt/mTOR signaling pathway.