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Published on: May 12, 2017
Ellagic acid promotes A549 cell apoptosis via regulating the phosphoinositide 3-kinase/protein kinase B pathway
Qiong Liu1, Xiaobing Liang1, Chengwei Niu1
1Medical Experiment Center, Xinhua College of Sun Yat-sen University, Guangzhou, Guangdong 510520, P.R. China.
Abstract:
The present study aimed to evaluate the anti-cancer effect of ellagic acid in human non-small cell lung cancer (NSCLC) A549 cells and to reveal the potential underlying mechanism. The effects of ellagic acid on the cell proliferation of A549 cells were determined by MTT assay. Cell cycle and apoptosis were measured with flow cytometry and Annexin V-propidium iodide staining. Western blotting was used to measure the expression levels of the phosphatidylinositol 3-kinase (PI3K)/protein kinas B (Akt) signaling pathway and apoptosis-associated proteins. It was demonstrated that ellagic acid exerted an inhibitory effect in the proliferation of human NSCLC A549 cells. Flow cytometry demonstrated that G1 phase retention and apoptosis rates were significantly increased after treatment with ellagic acid. Further investigation revealed that ellagic acid treatment diminished the phosphorylation of PI3K and Akt and regulated the expression of apoptosis-associated proteins in A549 cells. In conclusion, the present results indicated that ellagic acid suppresses cell proliferation, arrests cell cycle and induces apoptosis in human NSCLC A549 cells by inhibiting the PI3K/Akt signaling pathway.
Insights
Ellagic acid inhibits non-small cell lung cancer (NSCLC) A549 cell proliferation by arresting the cell cycle and inducing apoptosis. This occurs through the inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide.
- Identifying novel therapeutic agents with targeted mechanisms is crucial for improving patient outcomes.
- Ellagic acid, a natural polyphenol, has shown potential anti-cancer properties in various studies.
Purpose of the Study:
- To investigate the anti-cancer effects of ellagic acid on human NSCLC A549 cells.
- To elucidate the underlying molecular mechanisms, focusing on cell cycle regulation, apoptosis, and the PI3K/Akt signaling pathway.
Main Methods:
- MTT assay to assess cell proliferation inhibition.
- Flow cytometry for cell cycle analysis and apoptosis quantification (Annexin V/propidium iodide staining).
- Western blotting to evaluate the expression of PI3K/Akt pathway proteins and apoptosis-associated markers.
Main Results:
- Ellagic acid significantly inhibited the proliferation of A549 cells.
- Treatment with ellagic acid led to G1 phase cell cycle arrest and increased apoptosis rates.
- Ellagic acid reduced the phosphorylation of PI3K and Akt, and modulated apoptosis-related protein expression.
Conclusions:
- Ellagic acid demonstrates potent anti-cancer activity against NSCLC A549 cells.
- The mechanism involves suppression of cell proliferation, cell cycle arrest, and induction of apoptosis.
- Inhibition of the PI3K/Akt signaling pathway is a key mechanism underlying ellagic acid's anti-cancer effects in NSCLC.
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