Abstract
Flavokawain A (FKA), a major chalcone in kava extracts, has exhibited anti-proliferative and apoptotic effects in the prostate cancer. However, the molecular mechanism of FKA remains unclear. In this study, FKA induces cell apoptosis and cell cycle arrest in a G2M phase to prostate cancer cells. FKA interferes with tubulin polymerization and inhibits survivin expression in PC3 cells. Molecular docking simulation experiment finds that FKA can bind to colchicine binding sites that inhibit tubulin polymerization. FKA treatment regulates the glutamine metabolism pathway in PC3 cells by reducing intracellular glutamine, glutamic and proline. FKA treatment also decreases the GSH content by decreasing the activity of GSH synthetase (GSS) and increasing the activity of glutathione thiol transferase (GSTP1), which subsequently induces ROS production and PC3 cell apoptosis.
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