Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.
Identifieur interne : 000377 ( Ncbi/Merge ); précédent : 000376; suivant : 000378Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.
Auteurs : Zheng-Hai Tang [République populaire de Chine] ; Wen-Xiang Cao [République populaire de Chine] ; Min-Xia Su [République populaire de Chine] ; Xiuping Chen [République populaire de Chine] ; Jin-Jian Lu [République populaire de Chine]Source :
- Toxicology and applied pharmacology [ 1096-0333 ] ; 2017.
Descripteurs français
- KwdFr :
- Acrylamides, Antinéoplasiques (pharmacologie), Antinéoplasiques (usage thérapeutique), Apoptose (), Apoptose (physiologie), Autophagie (), Autophagie (physiologie), Carcinome pulmonaire non à petites cellules (métabolisme), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Cellules A549, Cellules HCT116, Dérivés de l'aniline, Espèces réactives de l'oxygène (métabolisme), Humains, Pipérazines (pharmacologie), Pipérazines (usage thérapeutique), Relation dose-effet des médicaments, Survie cellulaire (), Survie cellulaire (physiologie), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- métabolisme : Carcinome pulmonaire non à petites cellules, Espèces réactives de l'oxygène, Tumeurs du poumon.
- pharmacologie : Antinéoplasiques, Pipérazines.
- physiologie : Apoptose, Autophagie, Survie cellulaire.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- usage thérapeutique : Antinéoplasiques, Pipérazines.
- Acrylamides, Apoptose, Autophagie, Cellules A549, Cellules HCT116, Dérivés de l'aniline, Humains, Relation dose-effet des médicaments, Survie cellulaire.
English descriptors
- KwdEn :
- A549 Cells, Acrylamides, Aniline Compounds, Antineoplastic Agents (pharmacology), Antineoplastic Agents (therapeutic use), Apoptosis (drug effects), Apoptosis (physiology), Autophagy (drug effects), Autophagy (physiology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Survival (drug effects), Cell Survival (physiology), Dose-Response Relationship, Drug, HCT116 Cells, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Piperazines (pharmacology), Piperazines (therapeutic use), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , metabolism : Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Piperazines.
- chemical , therapeutic use : Antineoplastic Agents, Piperazines.
- chemical : Acrylamides, Aniline Compounds.
- drug effects : Apoptosis, Autophagy, Cell Survival.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- physiology : Apoptosis, Autophagy, Cell Survival.
- A549 Cells, Dose-Response Relationship, Drug, HCT116 Cells, Humans.
Abstract
Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation. Herein, we indicated for the first time that OSI increased the accumulations of cytoplasmic vacuoles, the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II), and the formation of GFP-LC3 puncta in various cancer cells. The OSI-induced expression of LC3-II was further increased when combined treatment with chloroquine (CQ), an autophagy inhibitor, and the mRFP-EGFP-LC3 plasmid-transfected cells exposed to OSI led to the production of more red-fluorescent puncta than green-fluorescent puncta, indicating OSI induced autophagic flux in the NSCLC cells. Knockdown of EGFR showed no effect on the OSI-induced expression of LC3-II in NCI-H1975 cells. In addition, OSI increased reactive oxygen species (ROS) generation and scavenge of ROS via pretreatment with N-acetyl-l-cysteine (NAC), catalase (CAT), or vitamin E (Vita E) significantly inhibited OSI-induced the accumulations of cytoplasmic vacuoles, the expression of LC3-II, as well as the formation of GFP-LC3 puncta. Combinative treatment with CQ could not remarkably change the OSI-induced cell viability decrease, whereas the OSI-induced cell viability decrease and apoptosis could be reversed through pretreatment with NAC, CAT, and Vita E, respectively. Taken together, this is the first report that OSI induces an accompanied autophagy and the generation of ROS is critical for the OSI-induced autophagy, cell viability decrease, and apoptosis in NSCLC cells.
DOI: 10.1016/j.taap.2017.02.017
PubMed: 28237877
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000174
- to stream PubMed, to step Curation: 000174
- to stream PubMed, to step Checkpoint: 000153
Links to Exploration step
pubmed:28237877Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.</title><author><name sortKey="Tang, Zheng Hai" sort="Tang, Zheng Hai" uniqKey="Tang Z" first="Zheng-Hai" last="Tang">Zheng-Hai Tang</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Wen Xiang" sort="Cao, Wen Xiang" uniqKey="Cao W" first="Wen-Xiang" last="Cao">Wen-Xiang Cao</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Su, Min Xia" sort="Su, Min Xia" uniqKey="Su M" first="Min-Xia" last="Su">Min-Xia Su</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Jin Jian" sort="Lu, Jin Jian" uniqKey="Lu J" first="Jin-Jian" last="Lu">Jin-Jian Lu</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. Electronic address: jinjianlu@umac.mo.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28237877</idno><idno type="pmid">28237877</idno><idno type="doi">10.1016/j.taap.2017.02.017</idno><idno type="wicri:Area/PubMed/Corpus">000174</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000174</idno><idno type="wicri:Area/PubMed/Curation">000174</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000174</idno><idno type="wicri:Area/PubMed/Checkpoint">000153</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000153</idno><idno type="wicri:Area/Ncbi/Merge">000377</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.</title><author><name sortKey="Tang, Zheng Hai" sort="Tang, Zheng Hai" uniqKey="Tang Z" first="Zheng-Hai" last="Tang">Zheng-Hai Tang</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Wen Xiang" sort="Cao, Wen Xiang" uniqKey="Cao W" first="Wen-Xiang" last="Cao">Wen-Xiang Cao</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Su, Min Xia" sort="Su, Min Xia" uniqKey="Su M" first="Min-Xia" last="Su">Min-Xia Su</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author><author><name sortKey="Lu, Jin Jian" sort="Lu, Jin Jian" uniqKey="Lu J" first="Jin-Jian" last="Lu">Jin-Jian Lu</name><affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. Electronic address: jinjianlu@umac.mo.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao</wicri:regionArea><wicri:noRegion>Macao</wicri:noRegion></affiliation></author></analytic><series><title level="j">Toxicology and applied pharmacology</title><idno type="eISSN">1096-0333</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Acrylamides</term><term>Aniline Compounds</term><term>Antineoplastic Agents (pharmacology)</term><term>Antineoplastic Agents (therapeutic use)</term><term>Apoptosis (drug effects)</term><term>Apoptosis (physiology)</term><term>Autophagy (drug effects)</term><term>Autophagy (physiology)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Cell Survival (drug effects)</term><term>Cell Survival (physiology)</term><term>Dose-Response Relationship, Drug</term><term>HCT116 Cells</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (metabolism)</term><term>Piperazines (pharmacology)</term><term>Piperazines (therapeutic use)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acrylamides</term><term>Antinéoplasiques (pharmacologie)</term><term>Antinéoplasiques (usage thérapeutique)</term><term>Apoptose ()</term><term>Apoptose (physiologie)</term><term>Autophagie ()</term><term>Autophagie (physiologie)</term><term>Carcinome pulmonaire non à petites cellules (métabolisme)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Cellules A549</term><term>Cellules HCT116</term><term>Dérivés de l'aniline</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Pipérazines (pharmacologie)</term><term>Pipérazines (usage thérapeutique)</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire ()</term><term>Survie cellulaire (physiologie)</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Piperazines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term><term>Piperazines</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Acrylamides</term><term>Aniline Compounds</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Espèces réactives de l'oxygène</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Pipérazines</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term><term>Pipérazines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Dose-Response Relationship, Drug</term><term>HCT116 Cells</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Acrylamides</term><term>Apoptose</term><term>Autophagie</term><term>Cellules A549</term><term>Cellules HCT116</term><term>Dérivés de l'aniline</term><term>Humains</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation. Herein, we indicated for the first time that OSI increased the accumulations of cytoplasmic vacuoles, the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II), and the formation of GFP-LC3 puncta in various cancer cells. The OSI-induced expression of LC3-II was further increased when combined treatment with chloroquine (CQ), an autophagy inhibitor, and the mRFP-EGFP-LC3 plasmid-transfected cells exposed to OSI led to the production of more red-fluorescent puncta than green-fluorescent puncta, indicating OSI induced autophagic flux in the NSCLC cells. Knockdown of EGFR showed no effect on the OSI-induced expression of LC3-II in NCI-H1975 cells. In addition, OSI increased reactive oxygen species (ROS) generation and scavenge of ROS via pretreatment with N-acetyl-l-cysteine (NAC), catalase (CAT), or vitamin E (Vita E) significantly inhibited OSI-induced the accumulations of cytoplasmic vacuoles, the expression of LC3-II, as well as the formation of GFP-LC3 puncta. Combinative treatment with CQ could not remarkably change the OSI-induced cell viability decrease, whereas the OSI-induced cell viability decrease and apoptosis could be reversed through pretreatment with NAC, CAT, and Vita E, respectively. Taken together, this is the first report that OSI induces an accompanied autophagy and the generation of ROS is critical for the OSI-induced autophagy, cell viability decrease, and apoptosis in NSCLC cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28237877</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0333</ISSN><JournalIssue CitedMedium="Internet"><Volume>321</Volume><PubDate><Year>2017</Year><Month>04</Month><Day>15</Day></PubDate></JournalIssue><Title>Toxicology and applied pharmacology</Title><ISOAbbreviation>Toxicol. Appl. Pharmacol.</ISOAbbreviation></Journal><ArticleTitle>Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>18-26</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0041-008X(17)30084-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.taap.2017.02.017</ELocationID><Abstract><AbstractText>Osimertinib (OSI), also known as AZD9291, is a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has been approved for the treatment of non-small cell lung cancer (NSCLC) patients harboring EGFR T790M mutation. Herein, we indicated for the first time that OSI increased the accumulations of cytoplasmic vacuoles, the expression of phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II), and the formation of GFP-LC3 puncta in various cancer cells. The OSI-induced expression of LC3-II was further increased when combined treatment with chloroquine (CQ), an autophagy inhibitor, and the mRFP-EGFP-LC3 plasmid-transfected cells exposed to OSI led to the production of more red-fluorescent puncta than green-fluorescent puncta, indicating OSI induced autophagic flux in the NSCLC cells. Knockdown of EGFR showed no effect on the OSI-induced expression of LC3-II in NCI-H1975 cells. In addition, OSI increased reactive oxygen species (ROS) generation and scavenge of ROS via pretreatment with N-acetyl-l-cysteine (NAC), catalase (CAT), or vitamin E (Vita E) significantly inhibited OSI-induced the accumulations of cytoplasmic vacuoles, the expression of LC3-II, as well as the formation of GFP-LC3 puncta. Combinative treatment with CQ could not remarkably change the OSI-induced cell viability decrease, whereas the OSI-induced cell viability decrease and apoptosis could be reversed through pretreatment with NAC, CAT, and Vita E, respectively. Taken together, this is the first report that OSI induces an accompanied autophagy and the generation of ROS is critical for the OSI-induced autophagy, cell viability decrease, and apoptosis in NSCLC cells.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Zheng-Hai</ForeName><Initials>ZH</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Wen-Xiang</ForeName><Initials>WX</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Min-Xia</ForeName><Initials>MX</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiuping</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Jin-Jian</ForeName><Initials>JJ</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China. Electronic address: jinjianlu@umac.mo.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Toxicol Appl Pharmacol</MedlineTA><NlmUniqueID>0416575</NlmUniqueID><ISSNLinking>0041-008X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000178">Acrylamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000814">Aniline Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010879">Piperazines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000596361">osimertinib</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000178" MajorTopicYN="N">Acrylamides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000814" MajorTopicYN="N">Aniline Compounds</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045325" MajorTopicYN="N">HCT116 Cells</DescriptorName></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="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010879" MajorTopicYN="N">Piperazines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">AZD9291</Keyword><Keyword MajorTopicYN="Y">Apoptosis</Keyword><Keyword MajorTopicYN="Y">Autophagy</Keyword><Keyword MajorTopicYN="Y">Osimertinib</Keyword><Keyword MajorTopicYN="Y">ROS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>02</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>02</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28237877</ArticleId><ArticleId IdType="pii">S0041-008X(17)30084-4</ArticleId><ArticleId IdType="doi">10.1016/j.taap.2017.02.017</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Tang, Zheng Hai" sort="Tang, Zheng Hai" uniqKey="Tang Z" first="Zheng-Hai" last="Tang">Zheng-Hai Tang</name></noRegion><name sortKey="Cao, Wen Xiang" sort="Cao, Wen Xiang" uniqKey="Cao W" first="Wen-Xiang" last="Cao">Wen-Xiang Cao</name><name sortKey="Chen, Xiuping" sort="Chen, Xiuping" uniqKey="Chen X" first="Xiuping" last="Chen">Xiuping Chen</name><name sortKey="Lu, Jin Jian" sort="Lu, Jin Jian" uniqKey="Lu J" first="Jin-Jian" last="Lu">Jin-Jian Lu</name><name sortKey="Su, Min Xia" sort="Su, Min Xia" uniqKey="Su M" first="Min-Xia" last="Su">Min-Xia Su</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Ncbi/Merge
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000377 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd -nk 000377 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Ncbi
|étape= Merge
|type= RBID
|clé= pubmed:28237877
|texte= Osimertinib induces autophagy and apoptosis via reactive oxygen species generation in non-small cell lung cancer cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:28237877" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |