Related Experiment Video
Updated: Apr 21, 2026
Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
Published on: August 21, 2019
Anti-proliferative effects of evodiamine in human lung cancer cells
Ji-Young Hong1, So Hyun Park1, Hye-Young Min1
1College of Pharmacy, Seoul National University, Seoul, Korea.
Background:
Evodiamine, a compound isolated from the Evodia rutaecarpa Bentham (Rutaceae), is known to have a potential anti-proliferative activity in human cancer cells. However, the growth inhibitory activity against lung cancer cells and the underlying molecular mechanisms have been poorly determined. The present study was designed to examine the anti-proliferative effect of evodiamine in A549 human lung cancer cells.
Methods:
A549 cells were treated with the compounds from Evodia rutaecarpa, and the anti-proliferative activity was evaluated by the sulforhodamine B assay. The mechanisms of action for the growth inhibitory activity of evodiamine on A549 human lung cancer cells were evaluated using flow cytometry for cell cycle distribution, and Western blot for assessment of accumulation and phosphorylation of potential target proteins.
Results:
Evodiamine exhibited a potent anti-proliferative activity against A549 human lung cancer cells. Flow cytometric analysis revealed that evodiamine induced cell cycle arrest at G2/M phase and apoptosis in the A549 cells. The cell cycle arrest was well correlated with the inhibition of cyclin B1, cyclin A, cdk2 and p-cdc2 (Tyr15) and increase of p-chk1 (Ser345) and p-chk2 (Thr68). Evodiamine also significantly increased the ratio of Bax/Bcl-2 and decreased procaspase-3, suggesting evodiamine-induced apoptosis via the intrinsic apoptotic pathway. In addition, evodiamine inhibited the expression of p-ERK and ERK.
Conclusions:
These findings suggest that the anti-proliferative effect of evodiamine was associated in part with the induction of G2/M phase cell cycle arrest and apoptosis, and down-regulation of ERK in human lung cancer cells.
Insights
Evodiamine effectively inhibits lung cancer cell growth by inducing cell cycle arrest and apoptosis. This compound also down-regulates ERK signaling pathways, offering potential for novel lung cancer therapies.
Area of Science:
- Pharmacology
- Molecular Biology
- Oncology
Background:
- Evodiamine, derived from Evodia rutaecarpa, shows potential anti-proliferative effects in cancer cells.
- The specific impact of evodiamine on lung cancer and its mechanisms remain largely uncharacterized.
Purpose of the Study:
- To investigate the anti-proliferative activity of evodiamine in A549 human lung cancer cells.
- To elucidate the molecular mechanisms underlying evodiamine's growth inhibitory effects.
Main Methods:
- Sulforhodamine B assay to assess anti-proliferative activity.
- Flow cytometry for cell cycle distribution analysis.
- Western blot to examine protein expression and phosphorylation.
Main Results:
- Evodiamine demonstrated significant anti-proliferative effects on A549 lung cancer cells.
- Evodiamine induced G2/M phase cell cycle arrest and apoptosis, evidenced by altered cyclin and caspase levels.
- Inhibition of ERK signaling and modulation of apoptosis-related proteins (Bax/Bcl-2) were observed.
Conclusions:
- Evodiamine's anti-proliferative action in lung cancer involves G2/M cell cycle arrest and apoptosis induction.
- Down-regulation of ERK signaling is a key mechanism contributing to evodiamine's efficacy.
- Evodiamine presents a potential therapeutic agent for human lung cancer.
