The cytotoxic effect and mechanism of Aralia elata were investigated in MDA-MB-231 human breast cancer cells. In this study, Aralia elata inhibited significantly the proliferation of MDA-MB-231 cells, and some typical apoptotic characteristics, such a...
The cytotoxic effect and mechanism of Aralia elata were investigated in MDA-MB-231 human breast cancer cells. In this study, Aralia elata inhibited significantly the proliferation of MDA-MB-231 cells, and some typical apoptotic characteristics, such as nuclear fragmentation and chromatin condensation, were observed. In addition, flow cytometry analysis showed that Aralia elata increased the sub-G1 (apoptosis) population and apoptosis further confirmed by Annexin V-FITC and PI double staining. With respect to the mechanism underlying the induction of apoptosis, apoptosis-related mRNA and proteins were measured using a reverse transcription-polymerase chain reaction and western blot analysis. Aralia elata reduced anti-apoptotic Bcl-2 mRNA and protein levels, but pro-apoptotic Bax mRNA and protein expression were increased compared with the controls. Aralia elata also induced the cleavage of caspase-9 followed by the activation of caspase-3, resulting in the activation of poly-ADP-ribose polymerase. These results suggest that apoptotic activity of Aralia elata is probably modulated by a caspase-dependent cascade via the activation of intrinsic pathway. This is the first report to demonstrate the cytotoxic effect of Aralia elata on human breast cancer cells and to provide a possible mechanism for this activity.