Abstract
Nasopharyngeal carcinoma (NPC) is one of the most common malignant head and neck cancers in southern China. Although the local and regional control of NPC has been considerably improved, patients with advanced disease still suffer from poor prognosis. Statins inhibit the mevalonate pathway and play antiproliferative and proapoptotic roles in a number of cancer cells. However, the effects and molecular mechanism of statins in NPC treatment remain unclear. In this study, the cell viability of NPC cell line, C666-1, after simvastatin exposure was determined using the alamarBlue Cell Viability Assay. Cell apoptosis in C666-1 treated with simvastatin was assessed by flow cytometry and TUNEL assay. The expression levels of cell cycle regulatory proteins were determined using western blotting. Simvastatin markedly decreased cell viability in a concentration-dependent manner, increased caspase 3 activity and induced apoptosis in C666-1 cells. Simvastatin induced Bim expression by regulating phosphorylation of transcriptional factor c-Jun. Simvastatin treatment induced cell cycle arrest in the G1 phase in C666-1 cells by inhibiting the expression of cyclin D1 and cyclin-dependent kinase 4, and enhancing p27 expression. Simvastatin treatment inhibited protein kinase B and extracellular signal regulated kinase 1/2 activation. In conclusion, the results of the present study reveal the possible molecular mechanism of simvastatin-induced anti-tumor effects in C666-1 and suggest that simvastatin is a potential chemotherapy agent in NPC treatment.