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Proteomic analysis reveals ATP-dependent steps and chaperones involvement in luteolin-induced lung cancer CH27 cell
Hong-Zin Lee1, Wen-Hui Yang, Bo-Ying Bao
1School of Pharmacy, China Medical University, Taichung, 91, Hsueh-Shih Road, Taichung, 40402, Taiwan. hong@mail.cmu.edu.tw
Abstract:
The present study applied 2D electrophoresis to analyze the proteins involved in luteolin (50 microM)-induced CH27 cell apoptosis. We found 7 proteins to be markedly changed. According to the data of analysis of these protein spots, we hypothesized that ATP synthetic pathway and heat shock proteins were involved in luteolin-induced CH27 cell apoptosis. In this study, luteolin induced a significant change in intracellular ATP levels and mitochondrial activity of CH27 cells. Further experiments demonstrated that pretreatment with forskolin blocked the luteolin-induced cell death. P38 and heat shock protein 27 may be important participants in the luteolin-induced changes in organization of actin microfilaments in this study. In addition, endoplasmic reticulum stress is also important in the luteolin-induced CH27 cell apoptosis. Our findings suggested that the function of mitochondria and endoplasmic reticulum is the integral factor in luteolin-induced CH27 cell apoptosis.
Insights
Luteolin triggers CH27 cell death by affecting ATP production and heat shock proteins. Mitochondrial and endoplasmic reticulum function are key to this apoptosis process.
Area of Science:
- Cell Biology
- Biochemistry
- Molecular Biology
Background:
- Luteolin, a plant flavonoid, has demonstrated potential anti-cancer properties.
- Understanding the molecular mechanisms of luteolin-induced apoptosis is crucial for its therapeutic development.
Purpose of the Study:
- To investigate the proteomic changes and molecular pathways involved in luteolin-induced apoptosis in CH27 cells.
- To elucidate the roles of mitochondria, endoplasmic reticulum, and specific proteins in this process.
Main Methods:
- Two-dimensional electrophoresis (2D electrophoresis) was employed to identify differentially expressed proteins.
- Intracellular ATP levels, mitochondrial activity, and actin microfilament organization were assessed.
- The effect of forskolin pretreatment on luteolin-induced cell death was evaluated.
Main Results:
- Seven proteins showed significant changes in expression following luteolin treatment.
- Luteolin significantly altered intracellular ATP levels and mitochondrial activity in CH27 cells.
- Endoplasmic reticulum stress and heat shock proteins (HSPs), including HSP27 and p38, were implicated in the apoptotic pathway.
Conclusions:
- Luteolin-induced apoptosis in CH27 cells involves alterations in ATP synthesis and heat shock protein pathways.
- Mitochondrial and endoplasmic reticulum functions are integral to luteolin's apoptotic effects.
- Forskolin pretreatment protected CH27 cells from luteolin-induced death, suggesting a role for cAMP signaling.
