Apoptotic effect of quercetin on HT-29 colon cancer cells via the AMPK signaling pathway
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Hyeong-Jin Kim1, Sang-Ki Kim, Byeong-Soo Kim
1Department of Companion and Laboratory Animal Science, Kongju National University, 340-702 Yesan, Republic of Korea.
Abstract:
Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. This study demonstrates the mechanism of quercetin-induced apoptosis in HT-29 colon cancer cells. Treatment of cells with quercetin significantly decreased cell viability in a dose-dependent manner. Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group. All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.
Insights
Quercetin triggers colon cancer cell death by activating AMP-activated protein kinase (AMPK) and p53. This natural compound shows potential as a chemopreventive or therapeutic agent for HT-29 colon cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- AMP-activated protein kinase (AMPK) is a key energy sensor that inhibits cell proliferation.
- Colon cancer, particularly the HT-29 cell line, remains a significant health concern requiring novel therapeutic strategies.
Purpose of the Study:
- To elucidate the mechanism by which quercetin induces apoptosis in HT-29 colon cancer cells.
- To investigate the role of AMPK activation and p53 in quercetin-mediated anti-cancer effects.
Main Methods:
- In vitro treatment of HT-29 cells with quercetin and assessment of cell viability, cell cycle, and apoptosis-related protein expression (AMPK, p53, p21).
- In vivo studies involving tumor xenografts in mice treated with quercetin to evaluate tumor volume reduction and protein induction.
Main Results:
- Quercetin significantly reduced HT-29 cell viability and induced G1 phase cell cycle arrest in a dose-dependent manner.
- Quercetin treatment upregulated apoptosis-related proteins, including AMPK, p53, and p21, within 48 hours.
- In vivo studies demonstrated quercetin's efficacy in reducing tumor volume and enhancing apoptosis-related protein expression.
Conclusions:
- Quercetin induces apoptosis in HT-29 colon cancer cells through AMPK activation and p53-dependent pathways.
- Quercetin exhibits potential as a chemopreventive or therapeutic agent for HT-29 colon cancer.
