Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells
Identifieur interne : 002D10 ( Main/Merge ); précédent : 002D09; suivant : 002D11Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells
Auteurs : Dae-Hee Lee [États-Unis] ; Dong-Wook Kim [États-Unis] ; Chang-Hwa Jung [Corée du Sud] ; Yong J. Lee [États-Unis] ; Daeho Park [Corée du Sud]Source :
- Toxicology and applied pharmacology [ 0041-008X ] ; 2014.
Descripteurs français
- KwdFr :
- Alcools gras (pharmacologie), Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (), Astrocytes (), Caspase-3 (métabolisme), Caspase-7 (métabolisme), Catéchols (pharmacologie), Espèces réactives de l'oxygène (métabolisme), Glioblastome (anatomopathologie), Humains, Ligand TRAIL (toxicité), Lignée cellulaire tumorale, Petit ARN interférent (pharmacologie), Protéines proto-oncogènes c-bcl-2 (métabolisme), Protéines régulatrices de l'apoptose (métabolisme), Récepteurs au TRAIL (biosynthèse).
- MESH :
- anatomopathologie : Glioblastome.
- biosynthèse : Récepteurs au TRAIL.
- métabolisme : Caspase-3, Caspase-7, Espèces réactives de l'oxygène, Protéines proto-oncogènes c-bcl-2, Protéines régulatrices de l'apoptose.
- pharmacologie : Alcools gras, Antinéoplasiques d'origine végétale, Catéchols, Petit ARN interférent.
- toxicité : Ligand TRAIL.
- Apoptose, Astrocytes, Humains, Lignée cellulaire tumorale.
English descriptors
- KwdEn :
- Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Apoptosis Regulatory Proteins (metabolism), Astrocytes (drug effects), Caspase 3 (metabolism), Caspase 7 (metabolism), Catechols (pharmacology), Cell Line, Tumor, Fatty Alcohols (pharmacology), Glioblastoma (pathology), Humans, Proto-Oncogene Proteins c-bcl-2 (metabolism), RNA, Small Interfering (pharmacology), Reactive Oxygen Species (metabolism), Receptors, TNF-Related Apoptosis-Inducing Ligand (biosynthesis), TNF-Related Apoptosis-Inducing Ligand (toxicity).
- MESH :
- chemical , biosynthesis : Receptors, TNF-Related Apoptosis-Inducing Ligand.
- chemical , metabolism : Apoptosis Regulatory Proteins, Caspase 3, Caspase 7, Proto-Oncogene Proteins c-bcl-2, Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Catechols, Fatty Alcohols, RNA, Small Interfering.
- drug effects : Apoptosis, Astrocytes.
- pathology : Glioblastoma.
- chemical , toxicity : TNF-Related Apoptosis-Inducing Ligand.
- Cell Line, Tumor, Humans.
Abstract
Glioblastoma multiforme (GBM) is the most lethal and aggressive astrocytoma of primary brain tumors in adults. Although there are many clinical trials to induce the cell death of glioblastoma cells, most glioblastoma cells have been reported to be resistant to TRAIL-induced apoptosis. Here, we showed that gingerol as a major component of ginger can induce TRAIL-mediated apoptosis of glioblastoma. Gingerol increased death receptor (DR) 5 levels in a p53-dependent manner. Furthermore, gingerol decreased the expression level of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and increased pro-apoptotic protein, Bax and truncate Bid, by generating reactive oxygen species (ROS).We also found that the sensitizing effects of gingerol in TRAIL-induced cell death were blocked by scavenging ROS or overexpressing anti-apoptotic protein (Bcl-2). Therefore, we showed the functions of gingerol as a sensitizing agent to induce cell death of TRAIL-resistant glioblastoma cells. This study gives rise to the possibility of applying gingerol as an anti-tumor agent that can be used for the purpose of combination treatment with TRAIL in TRAIL-resistant glioblastoma tumor therapy.
Url:
DOI: 10.1016/j.taap.2014.06.030
PubMed: 25034532
PubMed Central: 4295120
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PMC:4295120Le document en format XML
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Lee</name><affiliation wicri:level="4"><nlm:aff id="A1">Departments of Surgery and Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Surgery and Pharmacology and Cell Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Park, Daeho" sort="Park, Daeho" uniqKey="Park D" first="Daeho" last="Park">Daeho Park</name><affiliation wicri:level="1"><nlm:aff id="A4">School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Republic of Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712</wicri:regionArea><wicri:noRegion>Gwangju 500-712</wicri:noRegion></affiliation></author></analytic><series><title level="j">Toxicology and applied pharmacology</title><idno type="ISSN">0041-008X</idno><idno type="eISSN">1096-0333</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Agents, Phytogenic (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Astrocytes (drug effects)</term><term>Caspase 3 (metabolism)</term><term>Caspase 7 (metabolism)</term><term>Catechols (pharmacology)</term><term>Cell Line, Tumor</term><term>Fatty Alcohols (pharmacology)</term><term>Glioblastoma (pathology)</term><term>Humans</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>RNA, Small Interfering (pharmacology)</term><term>Reactive Oxygen Species (metabolism)</term><term>Receptors, TNF-Related Apoptosis-Inducing Ligand (biosynthesis)</term><term>TNF-Related Apoptosis-Inducing Ligand (toxicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alcools gras (pharmacologie)</term><term>Antinéoplasiques d'origine végétale (pharmacologie)</term><term>Apoptose ()</term><term>Astrocytes ()</term><term>Caspase-3 (métabolisme)</term><term>Caspase-7 (métabolisme)</term><term>Catéchols (pharmacologie)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Glioblastome (anatomopathologie)</term><term>Humains</term><term>Ligand TRAIL (toxicité)</term><term>Lignée cellulaire tumorale</term><term>Petit ARN interférent (pharmacologie)</term><term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term><term>Protéines régulatrices de l'apoptose (métabolisme)</term><term>Récepteurs au TRAIL (biosynthèse)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Receptors, TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apoptosis Regulatory Proteins</term><term>Caspase 3</term><term>Caspase 7</term><term>Proto-Oncogene Proteins c-bcl-2</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term><term>Catechols</term><term>Fatty Alcohols</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Glioblastome</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Récepteurs au TRAIL</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Astrocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Caspase-7</term><term>Espèces réactives de l'oxygène</term><term>Protéines proto-oncogènes c-bcl-2</term><term>Protéines régulatrices de l'apoptose</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Glioblastoma</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Alcools gras</term><term>Antinéoplasiques d'origine végétale</term><term>Catéchols</term><term>Petit ARN interférent</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>TNF-Related Apoptosis-Inducing Ligand</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Ligand TRAIL</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Astrocytes</term><term>Humains</term><term>Lignée cellulaire tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Glioblastoma multiforme (GBM) is the most lethal and aggressive astrocytoma of primary brain tumors in adults. Although there are many clinical trials to induce the cell death of glioblastoma cells, most glioblastoma cells have been reported to be resistant to TRAIL-induced apoptosis. Here, we showed that gingerol as a major component of ginger can induce TRAIL-mediated apoptosis of glioblastoma. Gingerol increased death receptor (DR) 5 levels in a p53-dependent manner. Furthermore, gingerol decreased the expression level of anti-apoptotic proteins (survivin, c-FLIP, Bcl-2, and XIAP) and increased pro-apoptotic protein, Bax and truncate Bid, by generating reactive oxygen species (ROS).We also found that the sensitizing effects of gingerol in TRAIL-induced cell death were blocked by scavenging ROS or overexpressing anti-apoptotic protein (Bcl-2). Therefore, we showed the functions of gingerol as a sensitizing agent to induce cell death of TRAIL-resistant glioblastoma cells. This study gives rise to the possibility of applying gingerol as an anti-tumor agent that can be used for the purpose of combination treatment with TRAIL in TRAIL-resistant glioblastoma tumor therapy.</p></div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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