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Effect of evodiamine on cell death pathways in human gastric cancer cells
Hanni Zhang1, Liping Liu2, Pingxiang Li2
1Department of Acupuncture, Wuhan Puren Hospital, Wuhan, Hubei, China.
Abstract:
Evodiamine (EVO) exerts anti-cancer effect in a majority of cancer cells. BGC-823 and SGC-7901 cells were used to study EVO-induced cytotoxicity in human gastric cancer cell. Our results demonstrated that EVO exposure elicited cell vialibility decrease and G2/M arrest caused by induction of cdc2/cyclin B1 complex activation. EVO also induced caspase-dependent apoptosis and necroptosis caused by induction of actication of RIP, RIP3 and MLKL. Moreover, increase of reactive oxygen species (ROS) levels and cytotoxicity induced by EVO were significantly attenuated by co-treatment with a ROS scavenger, EUK134. In conclusion, EVO induced ROS-dependent cytotoxicity, which may involve apoptosis and necroptosis, in human gastric cancer cells.
Insights
Evodiamine (EVO) shows anti-cancer effects by decreasing human gastric cancer cell viability and causing cell cycle arrest. EVO-induced cytotoxicity is linked to reactive oxygen species (ROS) production, apoptosis, and necroptosis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Evodiamine (EVO) is a natural alkaloid with demonstrated anti-cancer properties.
- Gastric cancer remains a significant global health challenge, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the cytotoxic mechanisms of Evodiamine (EVO) in human gastric cancer cell lines (BGC-823 and SGC-7901).
- To elucidate the role of reactive oxygen species (ROS), apoptosis, and necroptosis in EVO-induced cell death.
Main Methods:
- Cell viability assays were performed on BGC-823 and SGC-7901 cells treated with EVO.
- Cell cycle progression was analyzed to identify arrest points.
- Western blotting was used to assess the activation of key proteins involved in apoptosis (caspase-dependent) and necroptosis (RIP, RIP3, MLKL).
- Reactive oxygen species (ROS) levels were measured, and the effect of a ROS scavenger (EUK134) was evaluated.
Main Results:
- EVO exposure significantly reduced cell viability and induced G2/M phase arrest in gastric cancer cells.
- EVO treatment activated the cdc2/cyclin B1 complex, leading to cell cycle arrest.
- EVO triggered both caspase-dependent apoptosis and RIPK/MLKL-dependent necroptosis.
- Increased ROS levels were observed following EVO treatment, and these increases, along with cytotoxicity, were attenuated by EUK134.
Conclusions:
- Evodiamine induces ROS-dependent cytotoxicity in human gastric cancer cells.
- The observed cytotoxicity involves the induction of both apoptosis and necroptosis.
- EVO represents a potential therapeutic agent for gastric cancer, warranting further investigation into its detailed molecular pathways.
