p-HPEA-EDA, a phenolic compound of virgin olive oil, activates AMP-activated protein kinase to inhibit carcinogenesis
Khanal P, Oh WK, Yun HJ, Namgoong GM, Ahn SG, Kwon SM, Choi HK, Choi HS
Carcinogenesis · 71 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- People, plus animal or lab work
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Research Foundation
- Government
- National Research Foundation of Korea
- Government
- Ministry of Education, Science and Technology
- Grants
- National Research Foundation of Korea (R13-2003-009); Ministry of Education, Science and Technology (R13-2003-009)
Based on 3 listed funder(s).
Publication
- Published
- 2011-01-07 · Carcinogenesis · vol. 32 · issue 4 · pp. 545–553
- Publisher
- Oxford University Press
- Cited
- 98 citations · more than 97% of similar papers · 7.2× the field average
- Impact
- Top 10% most cited in its field
- References
- 51 works
- Access
- Free to read
- Research areas
- Inflammatory mediators and NSAID effects · Cholesterol and Lipid Metabolism · Cancer, Lipids, and Metabolism
- Keywords
- AMPK, Chemistry, Protein kinase A, Kinase, Phosphorylation, Activator (genetics), Biochemistry, Molecular biology, Cell biology, Biology, Receptor
- MeSH
- cell line, tumor, humans, cell transformation, neoplastic, aldehydes, tetradecanoylphorbol acetate, phenols, plant oils, antineoplastic agents, apoptosis, cell survival, enzyme activation, tumor suppressor protein p53, cyclooxygenase 2, amp-activated protein kinases, olive oil, cyclopentane monoterpenes
8 authors
From KR
- Pukar KhanalChosun University
- Won Keun OhChosun University
- H. J. YunChosun University
- Gwang Mo NamgoongChosun University
- Sang‐Gun AhnChosun University
- Sang‐Mo KwonChosun University
Abstract
Phenolic constituents of virgin olive oil are reported to have antitumor activity. However, the underlying molecular mechanisms and specific target proteins of virgin olive oil remain to be elucidated. Here, we report that dialdehydic form of decarboxymethyl ligstroside aglycone (p-HPEA-EDA), a phenolic compound of virgin olive oil, inhibits tumor promoter-induced cell transformation in JB6 Cl41 cells and suppress cyclooxygenase-2 (COX-2) and tumorigenicity by adenosine monophosphate-activated protein kinase (AMPK) activation in HT-29 cells. p-HPEA-EDA inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced phosphorylation of extracellular signal-regulated kinases 1/2 and p90RSK in JB6 Cl41 cells, resulting in the inhibition of cell proliferation, activator protein-1 transactivation and cell transformation promoted by TPA. Moreover, p-HPEA-EDA strongly inhibited the cell viability and COX-2 expression by activation of AMPK activity in HT-29 cells, resulted from depletion of intracellular adenosine triphosphate. p-HPEA-EDA-induced activation of caspase-3 and poly-adenosine diphosphate-ribose polymerase, phosphorylation of p53 (Ser15) and DNA fragmentation in HT-29 cells, leading to apoptosis. Importantly, p-HPEA-EDA suppressed the colony formation of HT-29 cells in soft agar. In contrast, Compound C, an AMPK inhibitor, and Z-DEVD-FMK, a caspase-3 inhibitor, blocked the p-HPEA-EDA-inhibited colony formation in HT-29 cells. In vivo chorioallantoic membrane assay also showed that p-HPEA-EDA-inhibited tumorigenicity of HT-29 cells. These findings revealed that targeted activation of AMPK and inhibition of COX-2 expression by p-HPEA-EDA contribute to the chemopreventive and chemotherapeutic potential of virgin olive oil against colon cancer cells.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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