Polyphenol elicits vital cellular responses (cytotoxicity, cell cycle arrest and apoptosis) through activating a cascade of molecular events. Curcumin (diferuloylmethane) is one of the polyphenols derived from tumeric, and is a rhizome of the plant Curcuma longa. In the past 50 years much research has showed that polyphenol can both prevent and treat cancer. However, the exact mechanism of its action on human bladder cancer cells is still unclear. We therefore investigated the mechanisms by which curcumin induced cell cycle arrest and apoptosis in human bladder cancer T24 cells in vitro. Assays were performed to determine cell viability, cell cycle arrest, apoptosis, caspases-3 activity and were measured and determined by flow cytometric assay, while gene expression was examined by polymerase chain reaction (PCR). Curcumin inhibited the expression of cyclin D1 and promoted the P53 and P21 expression that led to inhibit the complex of CDK1 and cyclin E before leading to G0/G1 arrest. The data also showed curcumin inhbited Bcl-2 expression and promoted Bak expression that led to decrease the mitochondria membrane potential that led to the release of cytochrome C and increased the caspase- 3 activity before leading to occurrence of apoptosis. Furthermore, the curcumin-induced apoptosis on T24 cells was blocked by the broad-spectrum caspase inhibitor (z-VAD-fmk).
