AMP kinase/cyclooxygenase-2 pathway regulates proliferation and apoptosis of cancer cells treated with quercetin.
10.3858/emm.2009.41.3.023
- Author:
Yun Kyoung LEE
1
;
Song Yi PARK
;
Young Min KIM
;
Won Sup LEE
;
Ock Jin PARK
Author Information
1. Department of Food and Nutrition, Hannam University Daedeok Valley Campus, Daejeon 305-811, Korea. ojpark@hnu.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
AMP-activated protein kinases;
apoptosis;
cyclooxygenase-2;
growth inhibitors;
HT-29 cells;
quercetin
- MeSH:
AMP-Activated Protein Kinases/antagonists & inhibitors/*physiology;
Anticarcinogenic Agents/*pharmacology;
Antioxidants/*pharmacology;
Apoptosis/*drug effects;
Cell Cycle/drug effects/physiology;
Cell Line, Tumor;
Cell Proliferation/*drug effects;
Cyclooxygenase 2/genetics/*physiology;
Cyclooxygenase 2 Inhibitors/pharmacology;
Enzyme Activation;
Humans;
Pyrazoles/pharmacology;
Pyrimidines/pharmacology;
Quercetin/*pharmacology
- From:Experimental & Molecular Medicine
2009;41(3):201-207
- CountryRepublic of Korea
- Language:English
-
Abstract:
AMPK (AMP-activated protein kinase) is highly conserved in eukaryotes, where it functions primarily as a sensor of cellular energy status. Recent studies indicate that AMPK activation strongly suppresses cell proliferation in non-malignant cells as well as in tumor cells. In this study, quercetin activated AMPK in MCF breast cancer cell lines and HT-29 colon cancer cells, and this activation of AMPK seemed to be closely related to a decrease in COX-2 expression. The application of a COX-2 inhibitor or cox-2(-/-) cells supported the idea that AMPK is an upstream signal of COX-2, and is required for the anti-proliferatory and pro-apoptotic effects of quercetin. The suppressive or growth inhibitory effects of quercetin on COX-2 were abolished by treating cancer cells with an AMPK inhibitor Compound C. These results suggest that AMPK is crucial to the anti-cancer effect of quercetin and that the AMPK-COX-2 signaling pathway is important in quercetin-mediated cancer control.
