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Recent studies showed that lncRNA  CASC9  was upregulated and acted as an oncogene in a variety of tumors. However, the expression and biological functions of  CASC9  in oral squamous cell carcinoma (OSCC) remain unknown. In this study, we found for the first time that  CASC9  was remarkably upregulated in OSCC tissues and cell lines compared with paired noncancerous tissues and normal oral epithelial cells. Highly expressed  CASC9  is strongly associated with tumor size, clinical stage, regional lymph node metastasis and overall survival time in OSCC patients. In vitro,  CASC9  knockdown in OSCC cells SCC15 and CAL27 significantly promotes autophagy and apoptosis, while inhibiting proliferation. Moreover, the expression levels of p-AKT, p-mTOR, P62 and BCL-2 were significantly decreased, while the expression levels of BAX and the LC3BII/LC3BI ratio were increased in  CASC9 -knockdown SCC15 and CAL27 cells. After the addition of the AKT activator SC79 in  CASC9 -knockdown SCC15 and CAL27 cells, we found that the increased autophagy and apoptosis were remarkably rescued. Furthermore, the increased apoptosis was remarkably rescued in  CASC9 -knockdown OSCC cells treated with the autophagy inhibitor Autophinib. In addition,  CASC9  depletion suppressed tumor growth in vivo. In conclusion, our findings demonstrate that lncRNA  CASC9  promotes OSCC progression through enhancing cell proliferation and suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway.  CASC9  could potentially be used as a valuable biomarker for OSCC diagnosis and prognosis.

cell death and disease

Increased expression of lncRNA CASC9 promotes tumor progression by suppressing autophagy-mediated cell apoptosis via the AKT/mTOR pathway in oral squamous cell carcinoma