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 : 000213 ( PubMed/Corpus ); précédent : 000212; suivant : 000214The 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 ; Tanja Bulat ; Igor Goli ; Sebastien Incerti ; Aleksandra Kora ; Ivan Petrovi ; Aleksandra Risti FiraSource :
- Cell biology and toxicology [ 1573-6822 ] ; 2016.
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
Links to Exploration step
pubmed:27026538Le document en format XML
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Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Incerti, Sebastien" sort="Incerti, Sebastien" uniqKey="Incerti S" first="Sebastien" last="Incerti">Sebastien Incerti</name><affiliation><nlm:affiliation>CNRS/IN2P3, Centre d'Etudes Nucléaires de Bordeaux Gradignan, CENBG, Université Bordeaux 1, 33175, Gradignan, France.</nlm:affiliation></affiliation></author><author><name sortKey="Kora, Aleksandra" sort="Kora, Aleksandra" uniqKey="Kora A" first="Aleksandra" last="Kora">Aleksandra Kora</name><affiliation><nlm:affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Petrovi, Ivan" sort="Petrovi, Ivan" uniqKey="Petrovi I" first="Ivan" last="Petrovi">Ivan Petrovi</name><affiliation><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation></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><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia. aristic@vin.bg.ac.rs.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27026538</idno><idno type="pmid">27026538</idno><idno type="doi">10.1007/s10565-016-9319-z</idno><idno type="wicri:Area/PubMed/Corpus">000213</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000213</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The impact of autophagy on cell death modalities in CRL-5876 lung adenocarcinoma cells after their exposure to γ-rays and/or erlotinib.</title><author><name sortKey="Keta, Otilija" sort="Keta, Otilija" uniqKey="Keta O" first="Otilija" last="Keta">Otilija Keta</name><affiliation><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Bulat, Tanja" sort="Bulat, Tanja" uniqKey="Bulat T" first="Tanja" last="Bulat">Tanja Bulat</name><affiliation><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Goli, Igor" sort="Goli, Igor" uniqKey="Goli I" first="Igor" last="Goli">Igor Goli</name><affiliation><nlm:affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Incerti, Sebastien" sort="Incerti, Sebastien" uniqKey="Incerti S" first="Sebastien" last="Incerti">Sebastien Incerti</name><affiliation><nlm:affiliation>CNRS/IN2P3, Centre d'Etudes Nucléaires de Bordeaux Gradignan, CENBG, Université Bordeaux 1, 33175, Gradignan, France.</nlm:affiliation></affiliation></author><author><name sortKey="Kora, Aleksandra" sort="Kora, Aleksandra" uniqKey="Kora A" first="Aleksandra" last="Kora">Aleksandra Kora</name><affiliation><nlm:affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</nlm:affiliation></affiliation></author><author><name sortKey="Petrovi, Ivan" sort="Petrovi, Ivan" uniqKey="Petrovi I" first="Ivan" last="Petrovi">Ivan Petrovi</name><affiliation><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</nlm:affiliation></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><nlm:affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia. aristic@vin.bg.ac.rs.</nlm:affiliation></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="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Erlotinib Hydrochloride</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="pathology" xml:lang="en"><term>Adenocarcinoma</term><term>Lung Neoplasms</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="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" 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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27026538</PMID><DateCompleted><Year>2017</Year><Month>02</Month><Day>02</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-6822</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>04</Month></PubDate></JournalIssue><Title>Cell biology and toxicology</Title><ISOAbbreviation>Cell Biol. Toxicol.</ISOAbbreviation></Journal><ArticleTitle>The impact of autophagy on cell death modalities in CRL-5876 lung adenocarcinoma cells after their exposure to γ-rays and/or erlotinib.</ArticleTitle><Pagination><MedlinePgn>83-101</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10565-016-9319-z</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Keta</LastName><ForeName>Otilija</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bulat</LastName><ForeName>Tanja</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Golić</LastName><ForeName>Igor</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Incerti</LastName><ForeName>Sebastien</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>CNRS/IN2P3, Centre d'Etudes Nucléaires de Bordeaux Gradignan, CENBG, Université Bordeaux 1, 33175, Gradignan, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Korać</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Faculty of Biology, University of Belgrade, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Petrović</LastName><ForeName>Ivan</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ristić-Fira</LastName><ForeName>Aleksandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001, Belgrade, Serbia. aristic@vin.bg.ac.rs.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>03</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Cell Biol Toxicol</MedlineTA><NlmUniqueID>8506639</NlmUniqueID><ISSNLinking>0742-2091</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>DA87705X9K</RegistryNumber><NameOfSubstance UI="D000069347">Erlotinib Hydrochloride</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000230" MajorTopicYN="N">Adenocarcinoma</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000532" MajorTopicYN="N">radiotherapy</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077192" MajorTopicYN="N">Adenocarcinoma of Lung</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053903" MajorTopicYN="N">DNA Breaks, Double-Stranded</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004260" MajorTopicYN="N">DNA Repair</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069347" MajorTopicYN="N">Erlotinib Hydrochloride</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005720" MajorTopicYN="N">Gamma Rays</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000532" MajorTopicYN="N">radiotherapy</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Erlotinib</Keyword><Keyword MajorTopicYN="N">Lung adenocarcinoma</Keyword><Keyword MajorTopicYN="N">Senescence</Keyword><Keyword MajorTopicYN="N">γ-rays</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>12</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>03</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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