Abstract
Objective:
This study aimed to explore the effect of quercetin on cervical cancer cells by inducing tumor endoplasmic reticulum stress (ERS) and apoptosis and its mechanism of action.
Methods:
HeLa cells were treated with different concentrations of quercetin, and the cell viability was measured using methyl thiazolyl tetrazolium (MTT) colorimetric assays. The apoptosis rate was measured using flow cytometry. The changes in the related protein X (Bax), B-cell lymphoma/leukemia-2 (Bcl-2), and G1/S-specific cyclin-D1 (Cyclin D1) levels after the HeLe apoptosis were determined using Western blot, and the changes in the human cystinase-3 (Caspase-3), glucoprotein 78 (GRP78), and enhancer-binding protein homologous protein (CHOP) levels, and the receptor-related protein levels in the ERS pathway/endoribonuclease inositol requiring enzyme 1 (IRE1), and the phosphorylated pancreatic endoplasmic reticulum stress kinase (p-Perk), and the activated transcription factor-6 (ATF6) levels were also quantified.
Results:
After treating the HeLa cells with different concentrations of quercetin, the cell viability was inhibited to varying degrees, showing a significant time and concentration dependence. The apoptosis rate in the quercetin group increased significantly in comparison with the blank control group, and the apoptosis rate also showed a tendency to increase progressively with an increasing concentration of the quercetin (P<0.05). The Bax and Bcl-2 levels in the quercetin intervention group showed a tendency to increase progressively in comparison with the blank control group, and Cyclin D1 showed a tendency to decrease progressively (P<0.05). The of Caspase-3, GRP78, and CHOP expression levels in the quercetin intervention group rose significantly in comparison with the blank control group (P<0.05). The IRE1, p-Perk, and c-ATF6 levels in the quercetin intervention group showed a tendency to rise gradually in comparison with the blank control group (P<0.05).
Conclusion:
Quercetin may promote the apoptosis of cervical cancer HeLe cells by inducing the tumor ERS pathway.
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