Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.
Identifieur interne : 000209 ( PubMed/Curation ); précédent : 000208; suivant : 000210Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.
Auteurs : Guixin Ma ; Weiwei Luo ; Jinjian Lu ; Dik-Lung Ma [Hong Kong] ; Chung-Hang Leung ; Yitao Wang ; Xiuping ChenSource :
- Chemico-biological interactions [ 1872-7786 ] ; 2016.
Descripteurs français
- KwdFr :
- Acétylcystéine (pharmacologie), Apoptose (), Autophagie (), Caspase-3 (métabolisme), Caspase-7 (métabolisme), Chloroquine (toxicité), Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire tumorale, Macrolides (toxicité), Microscopie de fluorescence, Poly(ADP-ribose) polymerases (métabolisme), Potentiel de membrane mitochondriale (), Prolifération cellulaire (), Protéines associées aux microtubules (métabolisme), Protéines proto-oncogènes c-bcl-2 (métabolisme), Synergie des médicaments, Technique de Western, Triterpènes (toxicité), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (métabolisme).
- MESH :
- anatomopathologie : Tumeurs du poumon.
- métabolisme : Caspase-3, Caspase-7, Espèces réactives de l'oxygène, Poly(ADP-ribose) polymerases, Protéines associées aux microtubules, Protéines proto-oncogènes c-bcl-2, Tumeurs du poumon.
- pharmacologie : Acétylcystéine.
- toxicité : Chloroquine, Macrolides, Triterpènes.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Microscopie de fluorescence, Potentiel de membrane mitochondriale, Prolifération cellulaire, Synergie des médicaments, Technique de Western.
English descriptors
- KwdEn :
- Acetylcysteine (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Blotting, Western, Caspase 3 (metabolism), Caspase 7 (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (toxicity), Drug Synergism, Humans, Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Macrolides (toxicity), Membrane Potential, Mitochondrial (drug effects), Microscopy, Fluorescence, Microtubule-Associated Proteins (metabolism), Poly(ADP-ribose) Polymerases (metabolism), Proto-Oncogene Proteins c-bcl-2 (metabolism), Reactive Oxygen Species (metabolism), Triterpenes (toxicity).
- MESH :
- chemical , metabolism : Caspase 3, Caspase 7, Microtubule-Associated Proteins, Poly(ADP-ribose) Polymerases, Proto-Oncogene Proteins c-bcl-2, Reactive Oxygen Species.
- chemical , pharmacology : Acetylcysteine.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Membrane Potential, Mitochondrial.
- metabolism : Lung Neoplasms.
- pathology : Lung Neoplasms.
- chemical , toxicity : Chloroquine, Macrolides, Triterpenes.
- Blotting, Western, Cell Line, Tumor, Drug Synergism, Humans, Microscopy, Fluorescence.
Abstract
Cucurbitacin E (CuE) is a triterpenoid with potent anticancer activities while the underlying mechanisms remain elusive. In the present study, the anticancer effects of CuE on 95D lung cancer cells were investigated. CuE decreased cell viability, inhibited colony formation, and increased reactive oxygen species (ROS) in a concentration-dependent manner, which were reversed by N-acetyl-l-cysteine (NAC). CuE induced apoptosis as determined by JC-1 staining, expression of Bcl-2 family proteins, cleavage of caspases, and TUNEL staining. NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP. Furthermore, CuE caused accumulation of autophagic vacuoles and concentration- and time-dependent expression of LC3II protein. Autophagy inhibitors chloroquine and bafilomycin A1 enhanced CuE-induced LC3II expression and cell death. CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment. In addition, CuE treatment damaged F-actin without affecting β-tubulin as confirmed by immunofluorescence. In conclusion, CuE induced ROS-dependent apoptosis through Bcl-2 family and caspases in 95D lung cancer cells. Furthermore, CuE induced protective autophagy mediated by ROS through AKT/mTOR pathway. This study provides novel roles of ROS in the anticancer effect of CuE.
DOI: 10.1016/j.cbi.2016.04.028
PubMed: 27106530
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Guixin Ma<affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation><affiliation><nlm:affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao. Electronic address: xpchen@umac.mo.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation>Le document en format XML
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Electronic address: xpchen@umac.mo.</nlm:affiliation><wicri:noCountry code="subField">Macao</wicri:noCountry></affiliation></author></analytic><series><title level="j">Chemico-biological interactions</title><idno type="eISSN">1872-7786</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Blotting, Western</term><term>Caspase 3 (metabolism)</term><term>Caspase 7 (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (toxicity)</term><term>Drug Synergism</term><term>Humans</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (pathology)</term><term>Macrolides (toxicity)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Microscopy, Fluorescence</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Poly(ADP-ribose) Polymerases (metabolism)</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Triterpenes (toxicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acétylcystéine (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Caspase-3 (métabolisme)</term><term>Caspase-7 (métabolisme)</term><term>Chloroquine (toxicité)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Macrolides (toxicité)</term><term>Microscopie de fluorescence</term><term>Poly(ADP-ribose) polymerases (métabolisme)</term><term>Potentiel de membrane mitochondriale ()</term><term>Prolifération cellulaire ()</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term><term>Synergie des médicaments</term><term>Technique de Western</term><term>Triterpènes (toxicité)</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term><term>Caspase 7</term><term>Microtubule-Associated Proteins</term><term>Poly(ADP-ribose) Polymerases</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>Acetylcysteine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term><term>Membrane Potential, Mitochondrial</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</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>Poly(ADP-ribose) polymerases</term><term>Protéines associées aux microtubules</term><term>Protéines proto-oncogènes c-bcl-2</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acétylcystéine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Chloroquine</term><term>Macrolides</term><term>Triterpenes</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Chloroquine</term><term>Macrolides</term><term>Triterpènes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blotting, Western</term><term>Cell Line, Tumor</term><term>Drug Synergism</term><term>Humans</term><term>Microscopy, Fluorescence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Microscopie de fluorescence</term><term>Potentiel de membrane mitochondriale</term><term>Prolifération cellulaire</term><term>Synergie des médicaments</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cucurbitacin E (CuE) is a triterpenoid with potent anticancer activities while the underlying mechanisms remain elusive. In the present study, the anticancer effects of CuE on 95D lung cancer cells were investigated. CuE decreased cell viability, inhibited colony formation, and increased reactive oxygen species (ROS) in a concentration-dependent manner, which were reversed by N-acetyl-l-cysteine (NAC). CuE induced apoptosis as determined by JC-1 staining, expression of Bcl-2 family proteins, cleavage of caspases, and TUNEL staining. NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP. Furthermore, CuE caused accumulation of autophagic vacuoles and concentration- and time-dependent expression of LC3II protein. Autophagy inhibitors chloroquine and bafilomycin A1 enhanced CuE-induced LC3II expression and cell death. CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment. In addition, CuE treatment damaged F-actin without affecting β-tubulin as confirmed by immunofluorescence. In conclusion, CuE induced ROS-dependent apoptosis through Bcl-2 family and caspases in 95D lung cancer cells. Furthermore, CuE induced protective autophagy mediated by ROS through AKT/mTOR pathway. This study provides novel roles of ROS in the anticancer effect of CuE. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27106530</PMID><DateCompleted><Year>2017</Year><Month>01</Month><Day>30</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7786</ISSN><JournalIssue CitedMedium="Internet"><Volume>253</Volume><PubDate><Year>2016</Year><Month>Jun</Month><Day>25</Day></PubDate></JournalIssue><Title>Chemico-biological interactions</Title><ISOAbbreviation>Chem. Biol. Interact.</ISOAbbreviation></Journal><ArticleTitle>Cucurbitacin E induces caspase-dependent apoptosis and protective autophagy mediated by ROS in lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>1-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cbi.2016.04.028</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0009-2797(16)30151-X</ELocationID><Abstract><AbstractText>Cucurbitacin E (CuE) is a triterpenoid with potent anticancer activities while the underlying mechanisms remain elusive. In the present study, the anticancer effects of CuE on 95D lung cancer cells were investigated. CuE decreased cell viability, inhibited colony formation, and increased reactive oxygen species (ROS) in a concentration-dependent manner, which were reversed by N-acetyl-l-cysteine (NAC). CuE induced apoptosis as determined by JC-1 staining, expression of Bcl-2 family proteins, cleavage of caspases, and TUNEL staining. NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP. Furthermore, CuE caused accumulation of autophagic vacuoles and concentration- and time-dependent expression of LC3II protein. Autophagy inhibitors chloroquine and bafilomycin A1 enhanced CuE-induced LC3II expression and cell death. CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment. In addition, CuE treatment damaged F-actin without affecting β-tubulin as confirmed by immunofluorescence. In conclusion, CuE induced ROS-dependent apoptosis through Bcl-2 family and caspases in 95D lung cancer cells. Furthermore, CuE induced protective autophagy mediated by ROS through AKT/mTOR pathway. This study provides novel roles of ROS in the anticancer effect of CuE. </AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Guixin</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Weiwei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Jinjian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Dik-Lung</ForeName><Initials>DL</Initials><AffiliationInfo><Affiliation>Department of Chemistry, Hong Kong Baptist University, Kowloon Tong, Hong Kong.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leung</LastName><ForeName>Chung-Hang</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yitao</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao.</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. Electronic address: xpchen@umac.mo.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>04</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Chem Biol Interact</MedlineTA><NlmUniqueID>0227276</NlmUniqueID><ISSNLinking>0009-2797</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477012">MAP1LC3A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018942">Macrolides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014315">Triterpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>88899-55-2</RegistryNumber><NameOfSubstance UI="C040929">bafilomycin A1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.4.2.30</RegistryNumber><NameOfSubstance UI="D011065">Poly(ADP-ribose) Polymerases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053148">Caspase 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053179">Caspase 7</NameOfSubstance></Chemical><Chemical><RegistryNumber>V8A45XYI21</RegistryNumber><NameOfSubstance UI="C102326">cucurbitacin E</NameOfSubstance></Chemical><Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber><NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053148" MajorTopicYN="N">Caspase 3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053179" MajorTopicYN="N">Caspase 7</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018942" MajorTopicYN="N">Macrolides</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053078" MajorTopicYN="N">Membrane Potential, Mitochondrial</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008856" MajorTopicYN="N">Microscopy, Fluorescence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011065" MajorTopicYN="N">Poly(ADP-ribose) Polymerases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014315" MajorTopicYN="N">Triterpenes</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Cancer</Keyword><Keyword MajorTopicYN="N">Cucurbitacin E</Keyword><Keyword MajorTopicYN="N">Reactive oxygen species</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>11</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>03</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>04</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>4</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>4</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>1</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27106530</ArticleId><ArticleId IdType="pii">S0009-2797(16)30151-X</ArticleId><ArticleId IdType="doi">10.1016/j.cbi.2016.04.028</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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