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

Li-Hong Zhu1, Wei Bi, Xiao-Dong Liu

  • 1Department of Pathophysiology, Medical College of Jinan University, and Department of Neurology, First Affiliated Hospital of Jinan University, Guangzhou 510632, PR China.

Oncology Reports
|September 3, 2011
PubMed

Insights

Evodiamine (Evo) inhibits gastric cancer cell growth by causing mitotic arrest and slippage. Sustained arrest is crucial for Evo to induce apoptosis, offering potential cancer treatment strategies.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Cancer Research

Background:

  • Evodiamine (Evo), an alkaloid from Evodia rutaecarpa, shows anti-proliferative and anti-tumor effects.
  • The precise mechanisms and molecular targets of Evo's anti-cancer activity remain largely unelucidated.
  • Understanding Evo's action is critical for its potential therapeutic applications in oncology.

Purpose of the Study:

  • To investigate the anti-proliferative and apoptotic mechanisms of Evodiamine (Evo) in human gastric cancer cells (SGC-7901).
  • To establish a cell synchronization model for detailed mechanistic studies of Evo.
  • To elucidate the role of mitotic arrest and mitotic slippage in Evo-induced apoptosis.

Main Methods:

  • Utilized a cell synchronization model in SGC-7901 human gastric cancer cells.
  • Transfected cells with full-length or non-degradable (ND) cyclinB1 to assess Evo's effects.
  • Investigated the impact of transient vs. sustained Evo treatment and CDK1 inhibition on apoptosis and mitotic events.

Main Results:

  • Evodiamine (Evo) significantly inhibited SGC-7901 cell proliferation and exhibited cytotoxicity.
  • Transient Evo treatment induced reversible mitotic arrest; sustained arrest (>16-20 hours) was necessary for apoptosis induction.
  • Promoting mitotic slippage enhanced apoptosis, while delaying it via ND cyclinB1 overexpression reduced Evo's apoptotic effects.

Conclusions:

  • Evodiamine (Evo)-induced apoptosis in gastric cancer cells is intrinsically linked to mitotic arrest and subsequent mitotic slippage.
  • The findings suggest that Evo's anti-cancer properties may stem from its ability to disrupt mitotic progression and induce cell death.
  • This study provides mechanistic insights into Evodiamine's potential as a therapeutic agent for cancer treatment and prevention.

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