The impact of autophagy on cell death modalities in CRL-5876 lung adenocarcinoma cells after their exposure to γ-rays and/or erlotinib.
Identifieur interne : 000D52 ( Main/Exploration ); précédent : 000D51; suivant : 000D53The impact of autophagy on cell death modalities in CRL-5876 lung adenocarcinoma cells after their exposure to γ-rays and/or erlotinib.
Auteurs : Otilija Keta [Serbie] ; Tanja Bulat [Serbie] ; Igor Goli [Serbie] ; Sebastien Incerti [France] ; Aleksandra Kora [Serbie] ; Ivan Petrovi [Serbie] ; Aleksandra Risti Fira [Serbie]Source :
- Cell biology and toxicology [ 1573-6822 ] ; 2016.
Descripteurs français
- KwdFr :
- Adénocarcinome (), Adénocarcinome (anatomopathologie), Adénocarcinome (radiothérapie), Adénocarcinome (traitement médicamenteux), Antinéoplasiques (pharmacologie), Apoptose (), Apoptose (effets des radiations), Autophagie (), Autophagie (effets des radiations), Cassures double-brin de l'ADN, Chlorhydrate d'erlotinib (pharmacologie), Chloroquine (pharmacologie), Cycle cellulaire (), Cycle cellulaire (effets des radiations), Humains, Lignée cellulaire tumorale, Rayons gamma (usage thérapeutique), Réparation de l'ADN, Tumeurs du poumon (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (radiothérapie), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- anatomopathologie : Adénocarcinome, Tumeurs du poumon.
- effets des radiations : Apoptose, Autophagie, Cycle cellulaire.
- pharmacologie : Antinéoplasiques, Chlorhydrate d'erlotinib, Chloroquine.
- radiothérapie : Adénocarcinome, Tumeurs du poumon.
- traitement médicamenteux : Adénocarcinome, Tumeurs du poumon.
- usage thérapeutique : Rayons gamma.
- Adénocarcinome, Apoptose, Autophagie, Cassures double-brin de l'ADN, Cycle cellulaire, Humains, Lignée cellulaire tumorale, Réparation de l'ADN, Tumeurs du poumon.
English descriptors
- KwdEn :
- Adenocarcinoma (drug therapy), Adenocarcinoma (pathology), Adenocarcinoma (radiotherapy), Adenocarcinoma (therapy), Adenocarcinoma of Lung, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Apoptosis (radiation effects), Autophagy (drug effects), Autophagy (radiation effects), Cell Cycle (drug effects), Cell Cycle (radiation effects), Cell Line, Tumor, Chloroquine (pharmacology), DNA Breaks, Double-Stranded, DNA Repair, Erlotinib Hydrochloride (pharmacology), Gamma Rays (therapeutic use), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Lung Neoplasms (radiotherapy), Lung Neoplasms (therapy).
- MESH :
- chemical , pharmacology : Antineoplastic Agents, Chloroquine, Erlotinib Hydrochloride.
- drug effects : Apoptosis, Autophagy, Cell Cycle.
- drug therapy : Adenocarcinoma, Lung Neoplasms.
- pathology : Adenocarcinoma, Lung Neoplasms.
- radiation effects : Apoptosis, Autophagy, Cell Cycle.
- radiotherapy : Adenocarcinoma, Lung Neoplasms.
- therapeutic use : Gamma Rays.
- therapy : Adenocarcinoma, Lung Neoplasms.
- Adenocarcinoma of Lung, Cell Line, Tumor, DNA Breaks, Double-Stranded, DNA Repair, Humans.
Abstract
In most patients with lung cancer radiation treatment is used either as single agent or in combination with radiosensitizing drugs. However, the mechanisms underlying combined therapy and its impact on different modes of cell death have not yet been fully elucidated. We aimed to examine effects of single and combined treatments with γ-rays and erlotinib on radioresistant CRL-5876 human lung adenocarcinoma cells with particular emphasis on cell death. CRL-5876 cells were treated with γ-rays and/or erlotinib and changes in cell cycle, DNA repair dynamics, ultrastructure, nuclear morphology and protein expression were monitored at different time points. To reveal the relationship between types of cell death that arise after these treatments, autophagy was blocked with chloroquine. We found that higher dose of γ-rays causes G2/M arrest while adding of erlotinib to this treatment decreases the number of cells in S phase. Impact of erlotinib on kinetics of disappearance of irradiation-induced DNA double strand breaks is reflected in the increase of residual γ-H2AX foci after 24 h. γ-rays provoke cytoprotective autophagy which precedes development of senescence. Erlotinib predominantly induces apoptosis and enlarges the number of apoptotic cells in the irradiated CRL-5876 cells. Chloroquine improved cytotoxicity induced by radiation and erlotinib, increased apoptosis and decreased senescence in the CRL-5876 cells. The results obtained on CRL-5876 cells indicate significant radiosensitizing effect of erlotinib and suggest that chloroquine in the combination with the above treatments may have an additional antitumor effect in lung adenocarcinoma.
DOI: 10.1007/s10565-016-9319-z
PubMed: 27026538
Affiliations:
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Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Goli, Igor" sort="Goli, Igor" uniqKey="Goli I" first="Igor" last="Goli">Igor Goli</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Faculty of Biology, University of Belgrade, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Incerti, Sebastien" sort="Incerti, Sebastien" uniqKey="Incerti S" first="Sebastien" last="Incerti">Sebastien Incerti</name><affiliation wicri:level="3"><nlm:affiliation>CNRS/IN2P3, Centre d'Etudes Nucléaires de Bordeaux Gradignan, CENBG, Université Bordeaux 1, 33175, Gradignan, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CNRS/IN2P3, Centre d'Etudes Nucléaires de Bordeaux Gradignan, CENBG, Université Bordeaux 1, 33175, Gradignan</wicri:regionArea><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Gradignan</settlement></placeName></affiliation></author><author><name sortKey="Kora, Aleksandra" sort="Kora, Aleksandra" uniqKey="Kora A" first="Aleksandra" last="Kora">Aleksandra Kora</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Faculty of Biology, University of Belgrade, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Petrovi, Ivan" sort="Petrovi, Ivan" uniqKey="Petrovi I" first="Ivan" last="Petrovi">Ivan Petrovi</name><affiliation wicri:level="1"><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author><author><name sortKey="Risti Fira, Aleksandra" sort="Risti Fira, Aleksandra" uniqKey="Risti Fira A" first="Aleksandra" last="Risti Fira">Aleksandra Risti Fira</name><affiliation wicri:level="1"><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia. aristic@vin.bg.ac.rs.</nlm:affiliation><country xml:lang="fr">Serbie</country><wicri:regionArea>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade</wicri:regionArea><wicri:noRegion>Belgrade</wicri:noRegion></affiliation></author></analytic><series><title level="j">Cell biology and toxicology</title><idno type="eISSN">1573-6822</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (drug therapy)</term><term>Adenocarcinoma (pathology)</term><term>Adenocarcinoma (radiotherapy)</term><term>Adenocarcinoma (therapy)</term><term>Adenocarcinoma of Lung</term><term>Antineoplastic Agents (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Apoptosis (radiation effects)</term><term>Autophagy (drug effects)</term><term>Autophagy (radiation effects)</term><term>Cell Cycle (drug effects)</term><term>Cell Cycle (radiation effects)</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>DNA Breaks, Double-Stranded</term><term>DNA Repair</term><term>Erlotinib Hydrochloride (pharmacology)</term><term>Gamma Rays (therapeutic use)</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (pathology)</term><term>Lung Neoplasms (radiotherapy)</term><term>Lung Neoplasms (therapy)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénocarcinome ()</term><term>Adénocarcinome (anatomopathologie)</term><term>Adénocarcinome (radiothérapie)</term><term>Adénocarcinome (traitement médicamenteux)</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose ()</term><term>Apoptose (effets des radiations)</term><term>Autophagie ()</term><term>Autophagie (effets des radiations)</term><term>Cassures double-brin de l'ADN</term><term>Chlorhydrate d'erlotinib (pharmacologie)</term><term>Chloroquine (pharmacologie)</term><term>Cycle cellulaire ()</term><term>Cycle cellulaire (effets des radiations)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Rayons gamma (usage thérapeutique)</term><term>Réparation de l'ADN</term><term>Tumeurs du poumon ()</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (radiothérapie)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Erlotinib Hydrochloride</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Adénocarcinome</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Cycle</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="effets des radiations" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Cycle cellulaire</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Chlorhydrate d'erlotinib</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Cycle</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="radiothérapie" xml:lang="fr"><term>Adénocarcinome</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="therapeutic use" xml:lang="en"><term>Gamma Rays</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Adénocarcinome</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Rayons gamma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Cell Line, Tumor</term><term>DNA Breaks, Double-Stranded</term><term>DNA Repair</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adénocarcinome</term><term>Apoptose</term><term>Autophagie</term><term>Cassures double-brin de l'ADN</term><term>Cycle cellulaire</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Réparation de l'ADN</term><term>Tumeurs du poumon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In most patients with lung cancer radiation treatment is used either as single agent or in combination with radiosensitizing drugs. However, the mechanisms underlying combined therapy and its impact on different modes of cell death have not yet been fully elucidated. We aimed to examine effects of single and combined treatments with γ-rays and erlotinib on radioresistant CRL-5876 human lung adenocarcinoma cells with particular emphasis on cell death. CRL-5876 cells were treated with γ-rays and/or erlotinib and changes in cell cycle, DNA repair dynamics, ultrastructure, nuclear morphology and protein expression were monitored at different time points. To reveal the relationship between types of cell death that arise after these treatments, autophagy was blocked with chloroquine. We found that higher dose of γ-rays causes G2/M arrest while adding of erlotinib to this treatment decreases the number of cells in S phase. Impact of erlotinib on kinetics of disappearance of irradiation-induced DNA double strand breaks is reflected in the increase of residual γ-H2AX foci after 24 h. γ-rays provoke cytoprotective autophagy which precedes development of senescence. Erlotinib predominantly induces apoptosis and enlarges the number of apoptotic cells in the irradiated CRL-5876 cells. Chloroquine improved cytotoxicity induced by radiation and erlotinib, increased apoptosis and decreased senescence in the CRL-5876 cells. The results obtained on CRL-5876 cells indicate significant radiosensitizing effect of erlotinib and suggest that chloroquine in the combination with the above treatments may have an additional antitumor effect in lung adenocarcinoma.</div></front></TEI><affiliations><list><country><li>France</li><li>Serbie</li></country><region><li>Aquitaine</li><li>Nouvelle-Aquitaine</li></region><settlement><li>Gradignan</li></settlement></list><tree><country name="Serbie"><noRegion><name sortKey="Keta, Otilija" sort="Keta, Otilija" uniqKey="Keta O" first="Otilija" last="Keta">Otilija Keta</name></noRegion><name sortKey="Bulat, Tanja" sort="Bulat, Tanja" uniqKey="Bulat T" first="Tanja" last="Bulat">Tanja Bulat</name><name sortKey="Goli, Igor" sort="Goli, Igor" uniqKey="Goli I" first="Igor" last="Goli">Igor Goli</name><name sortKey="Kora, Aleksandra" sort="Kora, Aleksandra" uniqKey="Kora A" first="Aleksandra" last="Kora">Aleksandra Kora</name><name sortKey="Petrovi, Ivan" sort="Petrovi, Ivan" uniqKey="Petrovi I" first="Ivan" last="Petrovi">Ivan Petrovi</name><name sortKey="Risti Fira, Aleksandra" sort="Risti Fira, Aleksandra" uniqKey="Risti Fira A" first="Aleksandra" last="Risti Fira">Aleksandra Risti Fira</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Incerti, Sebastien" sort="Incerti, Sebastien" uniqKey="Incerti S" first="Sebastien" last="Incerti">Sebastien Incerti</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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