Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways

Background: Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis. However, whether it also has anticancer activities in KOSC3 cells, an oral cancer cell line, is unclear. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and western blotting assays were carried out to assess cell viability, subG1 phase of the cell cycle, and apoptosis-related protein expression, respectively. Results: Our findings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers, including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells. Also, the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells. In addition, treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability. Moreover, caspase-8, caspase-9, caspase-7, and BH3 interacting domain death agonist (Bid) were activated in paclitaxel-treated KOSC3 cells. Conclusions: Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.