Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.
Identifieur interne : 000248 ( PubMed/Corpus ); précédent : 000247; suivant : 000249Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.
Auteurs : Ji-Hong Moon ; Seong Kug Eo ; John Hwa Lee ; Sang-Youel ParkSource :
- Oncology reports [ 1791-2431 ] ; 2015.
English descriptors
- KwdEn :
- Antineoplastic Agents (pharmacology), Autophagy (drug effects), Cell Line, Tumor, Chloroquine (pharmacology), Dose-Response Relationship, Drug, Gene Expression Regulation, Neoplastic (drug effects), Humans, Lung Neoplasms (metabolism), Microtubule-Associated Proteins (metabolism), Quercetin (pharmacology), RNA-Binding Proteins (metabolism), TNF-Related Apoptosis-Inducing Ligand (metabolism).
- MESH :
- chemical , metabolism : Microtubule-Associated Proteins, RNA-Binding Proteins, TNF-Related Apoptosis-Inducing Ligand.
- chemical , pharmacology : Antineoplastic Agents, Chloroquine, Quercetin.
- drug effects : Autophagy, Gene Expression Regulation, Neoplastic.
- metabolism : Lung Neoplasms.
- Cell Line, Tumor, Dose-Response Relationship, Drug, Humans.
Abstract
Quercetin is a potent cancer therapeutic agent and dietary antioxidant present in fruit and vegetables. Quercetin prevents tumor proliferation by inducing cell cycle arrest and is a well known cancer therapeutic agent and autophagy mediator. We investigated whether quercetin enhances TRAIL-induced tumor cell death and the possible mechanism in human lung cancer cells. We identified that quercetin markedly enhanced TRAIL-mediated lung cancer cell death. Quercetin treatment dose-dependently decreased the p62 protein expression and increased GFP-LC3B. Autophagy flux inhibitor, chloroquine treatment blocked the enhancing effects of TRAIL-induced apoptosis by quercetin. Our results indicated that quercetin enhanced TRAIL-induced cell death via autophagy flux activation, and also suggest that quercetin may be a therapeutic agent against human lung cancer via combination therapy with many anticancer drugs including TRAIL.
DOI: 10.3892/or.2015.3991
PubMed: 25997470
Links to Exploration step
pubmed:25997470Le document en format XML
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<author><name sortKey="Moon, Ji Hong" sort="Moon, Ji Hong" uniqKey="Moon J" first="Ji-Hong" last="Moon">Ji-Hong Moon</name>
<affiliation><nlm:affiliation>Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561-756, Republic of Korea.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Eo, Seong Kug" sort="Eo, Seong Kug" uniqKey="Eo S" first="Seong Kug" last="Eo">Seong Kug Eo</name>
<affiliation><nlm:affiliation>Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561-756, Republic of Korea.</nlm:affiliation>
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<author><name sortKey="Lee, John Hwa" sort="Lee, John Hwa" uniqKey="Lee J" first="John Hwa" last="Lee">John Hwa Lee</name>
<affiliation><nlm:affiliation>Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561-756, Republic of Korea.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Park, Sang Youel" sort="Park, Sang Youel" uniqKey="Park S" first="Sang-Youel" last="Park">Sang-Youel Park</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.</title>
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<term>Autophagy (drug effects)</term>
<term>Cell Line, Tumor</term>
<term>Chloroquine (pharmacology)</term>
<term>Dose-Response Relationship, Drug</term>
<term>Gene Expression Regulation, Neoplastic (drug effects)</term>
<term>Humans</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Quercetin (pharmacology)</term>
<term>RNA-Binding Proteins (metabolism)</term>
<term>TNF-Related Apoptosis-Inducing Ligand (metabolism)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Microtubule-Associated Proteins</term>
<term>RNA-Binding Proteins</term>
<term>TNF-Related Apoptosis-Inducing Ligand</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Chloroquine</term>
<term>Quercetin</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Gene Expression Regulation, Neoplastic</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
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<front><div type="abstract" xml:lang="en">Quercetin is a potent cancer therapeutic agent and dietary antioxidant present in fruit and vegetables. Quercetin prevents tumor proliferation by inducing cell cycle arrest and is a well known cancer therapeutic agent and autophagy mediator. We investigated whether quercetin enhances TRAIL-induced tumor cell death and the possible mechanism in human lung cancer cells. We identified that quercetin markedly enhanced TRAIL-mediated lung cancer cell death. Quercetin treatment dose-dependently decreased the p62 protein expression and increased GFP-LC3B. Autophagy flux inhibitor, chloroquine treatment blocked the enhancing effects of TRAIL-induced apoptosis by quercetin. Our results indicated that quercetin enhanced TRAIL-induced cell death via autophagy flux activation, and also suggest that quercetin may be a therapeutic agent against human lung cancer via combination therapy with many anticancer drugs including TRAIL. </div>
</front>
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<ArticleTitle>Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.</ArticleTitle>
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<Abstract><AbstractText>Quercetin is a potent cancer therapeutic agent and dietary antioxidant present in fruit and vegetables. Quercetin prevents tumor proliferation by inducing cell cycle arrest and is a well known cancer therapeutic agent and autophagy mediator. We investigated whether quercetin enhances TRAIL-induced tumor cell death and the possible mechanism in human lung cancer cells. We identified that quercetin markedly enhanced TRAIL-mediated lung cancer cell death. Quercetin treatment dose-dependently decreased the p62 protein expression and increased GFP-LC3B. Autophagy flux inhibitor, chloroquine treatment blocked the enhancing effects of TRAIL-induced apoptosis by quercetin. Our results indicated that quercetin enhanced TRAIL-induced cell death via autophagy flux activation, and also suggest that quercetin may be a therapeutic agent against human lung cancer via combination therapy with many anticancer drugs including TRAIL. </AbstractText>
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