Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.
Identifieur interne : 000E76 ( Main/Exploration ); précédent : 000E75; suivant : 000E77Quercetin-induced autophagy flux enhances TRAIL-mediated tumor cell death.
Auteurs : Ji-Hong Moon [Corée du Sud] ; Seong Kug Eo [Corée du Sud] ; John Hwa Lee [Corée du Sud] ; Sang-Youel Park [Corée du Sud]Source :
- Oncology reports [ 1791-2431 ] ; 2015.
Descripteurs français
- KwdFr :
- Antinéoplasiques (pharmacologie), Autophagie (), Chloroquine (pharmacologie), Humains, Ligand TRAIL (métabolisme), Lignée cellulaire tumorale, Protéines associées aux microtubules (métabolisme), Protéines de liaison à l'ARN (métabolisme), Quercétine (pharmacologie), Relation dose-effet des médicaments, Régulation de l'expression des gènes tumoraux (), Tumeurs du poumon (métabolisme).
- MESH :
- métabolisme : Ligand TRAIL, Protéines associées aux microtubules, Protéines de liaison à l'ARN, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques, Chloroquine, Quercétine.
- Autophagie, Humains, Lignée cellulaire tumorale, Relation dose-effet des médicaments, Régulation de l'expression des gènes tumoraux.
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
Affiliations:
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Le document en format XML
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561-756</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oncology reports</title><idno type="eISSN">1791-2431</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Agents (pharmacology)</term><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></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antinéoplasiques (pharmacologie)</term><term>Autophagie ()</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Ligand TRAIL (métabolisme)</term><term>Lignée cellulaire tumorale</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines de liaison à l'ARN (métabolisme)</term><term>Quercétine (pharmacologie)</term><term>Relation dose-effet des médicaments</term><term>Régulation de l'expression des gènes tumoraux ()</term><term>Tumeurs du poumon (métabolisme)</term></keywords><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" qualifier="métabolisme" xml:lang="fr"><term>Ligand TRAIL</term><term>Protéines associées aux microtubules</term><term>Protéines de liaison à l'ARN</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Chloroquine</term><term>Quercétine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Dose-Response Relationship, Drug</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Relation dose-effet des médicaments</term><term>Régulation de l'expression des gènes tumoraux</term></keywords></textClass></profileDesc></teiHeader><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></TEI><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Moon, Ji Hong" sort="Moon, Ji Hong" uniqKey="Moon J" first="Ji-Hong" last="Moon">Ji-Hong Moon</name></noRegion><name sortKey="Eo, Seong Kug" sort="Eo, Seong Kug" uniqKey="Eo S" first="Seong Kug" last="Eo">Seong Kug Eo</name><name sortKey="Lee, John Hwa" sort="Lee, John Hwa" uniqKey="Lee J" first="John Hwa" last="Lee">John Hwa Lee</name><name sortKey="Park, Sang Youel" sort="Park, Sang Youel" uniqKey="Park S" first="Sang-Youel" last="Park">Sang-Youel Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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