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KMID : 0620920090410030201
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Experimental & Molecular Medicine
2009 Volume.41 No. 3 p.201 ~ p.207
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AMP kinase/cyclooxygenase-2 pathway regulates proliferation and apoptosis of cancer cells treated with quercetin
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Lee Yun-Kyoung
Park Song-Yi
Kim Young-Min
Lee Won-Sup
Park Ock-Jin
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Abstract
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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.
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KEYWORD
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AMP-activated protein kinases, apoptosis, cyclooxygenase-2, growth inhibitors, HT-29 cells, quercetin
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