Triptolide suppresses the proliferation and induces the apoptosis of nasopharyngeal carcinoma cells via the PI3K/Akt pathway.

Nasopharyngeal carcinoma (NPC) is an endothelium-associated malignancy that is heavily influenced by Epstein Barr virus infection. Triptolide, extracted from Tripterygium wilfordii, has been proven to possess anti-inflammatory, immunosuppressive and anti-cancerous activity. Although the effect of triptolide on numerous cancer cell types has been outlined, its effect in NPC remained unclear. The present study investigated the effects and underlying mechanisms of triptolide in C666-1 and NP69 cells. It was revealed that triptolide significantly inhibited proliferation and induced apoptosis in C666-1 cells. Increased levels of cleaved-caspase-3 and apoptosis regulator BAX, decreased expression of apoptosis regulator Bcl-2, and reduced phosphorylation of RAC-α serine/threonine-protein kinase (Akt), were responsible for this induction of apoptosis. Notably, pretreating C666-1 cells with the phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor LY294002 suggested that with increasing concentrations of LY294002, triptolide exhibited decreasing ability to suppress proliferation and induce apoptosis in these cells. In conclusion, the results demonstrated that triptolide suppressed the proliferation and induced the apoptosis of C666-1 cells in a PI3K/Akt-dependent manner and therefore, may serve as a promising therapeutic candidate for NPC.