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Nasopharyngeal carcinoma (NPC) is a rare malignancy with a remarkable geographical distribution. Regarding NPC treatment, improving the survival rate of advanced patients seems promising. Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway deregulation is closely associated with tumorigenesis. In the present study, the NPC cell line SUNE1 was divided into four groups: Control, NVP-BEZ235, rapamycin, and NVP-BEZ235+rapamycin. SUNE1 cells in the NVP-BEZ235 group were incubated with NVP-BEZ235; cells in the rapamycin group were incubated with rapamycin, whereas the NVP-BEZ235+rapamycin group refers to SUNE1 cells incubated with a mixture of NVP-BEZ235 and rapamycin. The control group was treated with the same amount of vehicle. Morphological, MTT, terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling and flow cytometry assays demonstrated that NVP-BEZ235 and rapamycin caused morphological changes, inhibited cell viability and induced cellular apoptosis. In addition, reverse transcription-quantitative polymerase chain reaction and western blot revealed that the combination of NVP-BEZ235 and rapamycin affected the activation of the PI3K/AKT/mTOR pathway. The combination of NVP-BEZ235 and rapamycin significantly improved the effect of the drug therapy. The potential underlying mechanism may comprise the joint effects of inhibiting cell viability, promoting cellular apoptosis and reducing relative signal protein expression levels in SUNE1 cells. These findings provided novel evidence that NVP-BEZ235 suppresses NPC development, and indicated a promising potential application of combination drug therapy (NVP-BEZ235+rapamycin) for the clinical treatment of NPC.

The combination of NVP‑BEZ235 and rapamycin regulates nasopharyngeal carcinoma cell viability and apoptosis via the PI3K/AKT/mTOR pathway