Apoptotic death in curcumin-treated NPC-TW 076 human nasopharyngeal carcinoma cells is mediated through the ROS, mitochondrial depolarization and caspase-3-dependent signaling responses

Curcumin, a potent candidate anticancer agent, is a dietary pigment (phenolic compound) derived from the food flavoring spice turmeric (Curcuma longa), and it has been shown to have inhibitory effects on tumor cells through antiproliferative and proapoptotic activities. However, there is no report showing curcumin-induced apoptotic cell death in human nasopharyngeal carcinoma cells in vitro. Thus, this study was performed to elucidate whether mitochondria and caspase cascades are involved in the modulation of apoptosis and cell cycle arrest in curcumin-treated NPC-TW 076 human nasopharyngeal carcinoma cells. The effects of curcumin on cell cycle arrest and apoptosis were measured by flow cytometry, and caspase-3 activity, apoptosis-associated protein levels and its regulated molecules were studied by flow cytometric assay and immunoblots. The results indicated that curcumin-induced G2/M phase arrest was associated with a marked decrease in the protein expression of cyclin A, cyclin B and cyclin-dependent kinase 1 (Cdk1). Curcumin-induced apoptosis was accompanied with upregulation of the protein expression of Bax and downregulation of the protein levels of Bcl-2, resulting in dysfunction of mitochondria and subsequently led to cytochrome c release and sequential activation of caspase-9 and caspase-3 in NPC-TW 076 cells in a time-dependent manner. These findings revealed that mitochondria, AIF caspase-3-dependent pathways play a vital role in curcumin-induced G2/M phase arrest and apoptosis of NPC-TW 076 cells ill vitro.