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Evodiamine (Evo) is an indole quinazoline alkaloid isolated from the fruitof Evodia rutaecarpa Bentham. Previous studies have shown that Evo exhibits anti-proliferativeanti-tumor activities in several cancer types, but its target(s) and underlyingmechanism(s) of action remain unclear. In the present study, we sought to establisha cell synchronization model in order to examine the anti-proliferative and apoptoticmechanisms of Evo in the human gastric cancer cell line SGC-7901. In addition,we transfected these cells with full-length or non-degradable (ND) cyclinB1 toevaluate the relationship between the induction of apoptosis and activation ofmitotic arrest and mitotic slippage by Evo. Our results demonstrated that Evomarkedly inhibited cell growth and was cytotoxic to SGC-7901 cells. Furthermore,transient Evo treatment (&lt;16 h) caused reversible mitotic arrest, but sustainedmitotic arrest was required to initiate apoptosis. The time required to reversethe apoptotic effects of Evo was between 16 and 20 h. We also demonstrated thatpromotion of mitotic slippage by a CDK1 inhibitor enhanced apoptosis. Furthermore,we evaluated the effect of delaying mitotic slippage by overexpressing ND cyclinB1,which delayed apoptosis. In conclusion, these results indicate that Evo-inducedapoptosis is associated with mitotic arrest and subsequent mitotic slippage, whichmay underlie the actions of Evo in the treatment and prevention of cancer.

Induction of apoptosis by evodiamine involves both activation of mitotic arrest and mitotic slippage