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Quercetin suppresses HeLa cell viability via AMPK-induced HSP70 and EGFR down-regulation
Jin Hee Jung1, Jeong Ok Lee, Ji Hae Kim
1Department of Anatomy, Korea University College of Medicine, Seongbuk-gu, Seoul 136-701, South Korea.
Abstract:
Quercetin, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells, although the mechanism is not completely understood. In this study, we found that quercetin increased the phosphorylation of AMP-activated protein kinase (AMPK) and downstream acetyl-CoA carboxylase (ACC) and suppressed the viability of HeLa cells. AICAR, an AMPK activator, and quercetin down-regulated heat shock protein (HSP)70 and increased the activity of the pro-apoptotic effector, caspase 3. Knock-down of AMPK blocked quercetin-mediated HSP70 down-regulation. Moreover, knock-down of HSP70 enhanced quercetin-mediated caspase 3 activation. Furthermore, quercetin sustained epidermal growth factor receptor (EGFR) activation by suppressing the phosphatases, PP2a and SHP-2. Finally, quercetin increased the interaction between EGFR and Cbl, and also induced the tyrosine phosphorylation of Cbl. Together, these results suggest that quercetin may have anti-tumor effects on HeLa cells via AMPK-induced HSP70 and down-regulation of EGFR.
Insights
Quercetin, an antioxidant, combats HeLa cancer cells by activating AMP-activated protein kinase (AMPK) and down-regulating heat shock protein 70 (HSP70). This flavonoid also impacts epidermal growth factor receptor (EGFR) signaling, suggesting anti-tumor potential.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Quercetin, a plant flavonoid, exhibits antioxidant properties and potential chemopreventive effects against cancer.
- The precise mechanisms underlying quercetin's anti-cancer activity remain incompletely elucidated.
Purpose of the Study:
- To investigate the molecular mechanisms by which quercetin exerts anti-tumor effects on HeLa cells.
- To explore the roles of AMP-activated protein kinase (AMPK), heat shock protein 70 (HSP70), and epidermal growth factor receptor (EGFR) in quercetin's action.
Main Methods:
- Cell viability assays were performed on HeLa cells treated with quercetin and AICAR (an AMPK activator).
- Western blotting and knockdown experiments were used to assess protein phosphorylation, expression levels (AMPK, acetyl-CoA carboxylase, HSP70, caspase 3, EGFR, Cbl), and protein interactions.
- Enzyme activity assays were conducted for caspase 3 and phosphatases (PP2a, SHP-2).
Main Results:
- Quercetin treatment increased AMPK and acetyl-CoA carboxylase phosphorylation, suppressed HeLa cell viability, and reduced HSP70 levels.
- Quercetin and AICAR elevated caspase 3 activity; AMPK knockdown abrogated quercetin-induced HSP70 downregulation, while HSP70 knockdown enhanced caspase 3 activation.
- Quercetin sustained EGFR activation by inhibiting PP2a and SHP-2, increased EGFR-Cbl interaction, and induced Cbl tyrosine phosphorylation.
Conclusions:
- Quercetin demonstrates anti-tumor effects on HeLa cells, mediated through the AMPK-HSP70 pathway.
- Quercetin's modulation of EGFR signaling, including sustained activation and Cbl phosphorylation, contributes to its anti-cancer activity.
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