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Zeaxanthin Induces Apoptosis via ROS-Regulated MAPK and AKT Signaling Pathway in Human Gastric Cancer Cells
Ya-Nan Sheng1, Ying-Hua Luo2, Shao-Bin Liu3
1Department of Food Science and Engineering, College of Food Science, Heilongjiang Bayi Agricultural University, Daqing 163319, People's Republic of China.
Background:
Zeaxanthin, a carotenoid commonly found in plants, has a variety of biological functions including anti-cancer activity.
Purpose:
This study aimed to investigate the potential mechanisms of zeaxanthin in human gastric cancer cells.
Methods:
CCK-8 assay was used to examine the cytotoxic effect of zeaxanthin on human gastric cancer cells. Flow cytometry was used to analyse AGS cell cycle distribution and apoptosis status. Western blot analysis was used to detect the expression levels of cycle-related proteins (Cyclin A, Cyclin B1, CDK1/2, p21, and p27), apoptosis-related proteins (Bcl-2, Bad, caspase-3, PARP), MAPK, AKT, STAT3, and NF-κB.
Results:
CCK-8 assay showed that zeaxanthin has obvious cytotoxic effects on 12 types of human gastric cancer cells, but no obvious toxic effect on normal cells. In addition, flow cytometry and Western blotting results showed that zeaxanthin induces apoptosis by reducing mitochondrial membrane potential; increasing Cytochrome C, Bax, cleaved-caspase-3 (cle-cas-3), and cleaved-PARP (cle-PARP) expression levels; and decreasing Bcl-2, pro-caspase-3 (pro-cas-3), and pro-PARP expression levels. Additionally, zeaxanthin caused cell cycle arrest at the G2/M phase by increasing the levels of p21 and p27 and reduced the levels of AKT, Cyclin A, Cyclin B1, and Cyclin-dependent kinase 1/2 (CDK1/2). Furthermore, after zeaxanthin treatment, the expression levels of reactive oxygen species (ROS), p-JNK, p-p38, and I-κB increased, and the expression levels of p-ERK, p-AKT, STAT3, and NF-κB decreased. However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-κB and STAT3, and reduced their protein expression levels.
Conclusion:
Zeaxanthin has a potential effect against gastric cancer cells through the ROS-mediated MAPK, AKT, NF-κB, and STAT3 signaling pathways, and it is expected to become a new drug for the treatment of human gastric cancer.
Insights
Zeaxanthin exhibits cytotoxic effects on gastric cancer cells by inducing apoptosis and cell cycle arrest. This natural compound shows promise as a potential therapeutic agent for human gastric cancer.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Research
Background:
- Zeaxanthin, a plant-derived carotenoid, possesses known biological functions, including anti-cancer properties.
- Investigating zeaxanthin's specific mechanisms in human gastric cancer is crucial for therapeutic development.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying zeaxanthin's effects on human gastric cancer cells.
- To determine zeaxanthin's potential as a novel therapeutic agent for gastric cancer.
Main Methods:
- Cytotoxicity was assessed using the CCK-8 assay.
- Cell cycle distribution and apoptosis were analyzed via flow cytometry.
- Protein expression levels of key cell cycle regulators, apoptosis markers, and signaling pathway components (MAPK, AKT, STAT3, NF-κB) were determined by Western blot analysis.
Main Results:
- Zeaxanthin demonstrated significant cytotoxic effects on multiple human gastric cancer cell lines with no observed toxicity in normal cells.
- Zeaxanthin induced apoptosis by altering mitochondrial membrane potential and modulating apoptosis-related proteins (e.g., increased Bax, cleaved-caspase-3; decreased Bcl-2).
- Zeaxanthin caused G2/M phase cell cycle arrest and modulated cell cycle proteins (e.g., increased p21, p27; decreased Cyclin B1, CDK1/2), involving reactive oxygen species (ROS) and the MAPK/AKT/NF-κB/STAT3 pathways.
Conclusions:
- Zeaxanthin exerts anti-gastric cancer effects by activating ROS-mediated signaling pathways, including MAPK, AKT, NF-κB, and STAT3.
- Zeaxanthin's ability to induce apoptosis and cell cycle arrest suggests its potential as a novel therapeutic candidate for human gastric cancer.
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