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Published on: September 3, 2013
Anti-proliferative effects of evodiamine on human prostate cancer cell lines DU145 and PC3
Shu-Fen Kan1, Ching-Han Yu, Hsiao-Fung Pu
1Department of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan, Republic of China.
Abstract:
Prostate carcinoma is one of the most common malignant tumors and has become a more common cancer in men. Previous studies demonstrated that evodiamine (EVO) exhibited anti-tumor activities on several cancers, but its effects on androgen-independent prostate cancer are unclear. In the present study, the action mechanisms of EVO on the growth of androgen-independent prostate cancer cells (DU145 and PC3 cells) were explored. EVO dramatically inhibited the growth and elevated cytotoxicity of DU145 and PC3 cells. The flow cytometric analysis of EVO-treated cells indicated a block of G2/M phase and an elevated level of DNA fragmentation. The G2/M arrest was accompanied by elevated Cdc2 kinase activity, an increase in expression of cyclin B1 and phosphorylated Cdc2 (Thr 161), and a decrease in expression of phosphorylated Cdc2 (Tyr 15), Myt-1, and interphase Cdc25C. TUNEL examination showed that EVO-induced apoptosis was observed at 72 h. EVO elevated the activities of caspase 3, 8, and 9 in DU145 cells, while in PC3 cells only the activities of caspase 3 and 9 were elevated. EVO also triggered the processing of caspase 3 and 9 in both DU145 and PC3 cells. We demonstrate that roscovitine treatment result in the reversion of G2/M arrest in response to EVO in both DU145 and PC3. However, inhibitory effect of roscovitine on EVO-induced apoptosis could only be observed in DU145 rather than PC3. In DU145, G2/M arrest might be a signal for initiation of EVO-triggered apoptosis. Whereas EVO-triggered PC3 apoptosis might be independent of G2/M arrest. These results suggested that EVO inhibited the growth of prostate cancer cell lines, DU145 and PC3, through an accumulation at G2/M phase and an induction of apoptosis.
Insights
Evodiamine (EVO) significantly inhibits growth and increases cancer cell death in androgen-independent prostate cancer cell lines. EVO induces G2/M cell cycle arrest and apoptosis, offering potential therapeutic strategies for prostate cancer.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Prostate carcinoma is a prevalent cancer in men.
- Evodiamine (EVO) shows anti-tumor potential, but its effect on androgen-independent prostate cancer is not well-understood.
Purpose of the Study:
- To investigate the mechanisms of EVO's action on androgen-independent prostate cancer cell lines (DU145 and PC3).
Main Methods:
- Cell viability assays, flow cytometry for cell cycle analysis and DNA fragmentation, Western blotting for cell cycle regulatory proteins, TUNEL assay for apoptosis, and caspase activity assays.
- Roscovitine was used to investigate the role of G2/M arrest in EVO-induced apoptosis.
Main Results:
- EVO significantly inhibited DU145 and PC3 cell growth and increased cytotoxicity.
- EVO induced G2/M cell cycle arrest and apoptosis, evidenced by DNA fragmentation and caspase activation.
- EVO modulated key proteins involved in G2/M phase regulation (e.g., cyclin B1, Cdc2, Myt-1, Cdc25C).
- Roscovitine reversed G2/M arrest but only inhibited EVO-induced apoptosis in DU145 cells, suggesting distinct apoptosis pathways in DU145 and PC3 cells.
Conclusions:
- EVO inhibits androgen-independent prostate cancer cell growth via G2/M arrest and apoptosis induction.
- The role of G2/M arrest in EVO-induced apoptosis differs between DU145 and PC3 cell lines.
