Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.
Identifieur interne : 000230 ( PubMed/Curation ); précédent : 000229; suivant : 000231Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.
Auteurs : E. Salas [États-Unis] ; S. Roy [États-Unis] ; T. Marsh [États-Unis] ; B. Rubin [États-Unis] ; J. Debnath [États-Unis]Source :
- Oncogene [ 1476-5594 ] ; 2016.
Descripteurs français
- KwdFr :
- Antipaludiques (pharmacologie), Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Chloroquine (pharmacologie), Humains, Lignée cellulaire tumorale, Mutation, Oxydoréduction (), Prolifération cellulaire (), Protéine p53 suppresseur de tumeur (métabolisme), Protéines proto-oncogènes p21(ras) (génétique), Tumeurs du poumon (anatomopathologie), Voie des pentoses phosphates ().
- MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- génétique : Protéines proto-oncogènes p21(ras).
- métabolisme : Protéine p53 suppresseur de tumeur.
- pharmacologie : Antipaludiques, Chloroquine.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Mutation, Oxydoréduction, Prolifération cellulaire, Voie des pentoses phosphates.
English descriptors
- KwdEn :
- Antimalarials (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Humans, Lung Neoplasms (pathology), Mutation, Oxidation-Reduction (drug effects), Pentose Phosphate Pathway (drug effects), Proto-Oncogene Proteins p21(ras) (genetics), Tumor Suppressor Protein p53 (metabolism).
- MESH :
- chemical , genetics : Proto-Oncogene Proteins p21(ras).
- chemical , metabolism : Tumor Suppressor Protein p53.
- chemical , pharmacology : Antimalarials, Chloroquine.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Oxidation-Reduction, Pentose Phosphate Pathway.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Humans, Mutation.
Abstract
Despite immense interest in using antimalarials as autophagy inhibitors to treat cancer, it remains unclear whether these agents act predominantly via autophagy inhibition or whether other pathways direct their anti-cancer properties. By comparing the treatment effects of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demonstrate that inhibition of the oxidative arm of the pentose phosphate pathway (oxPPP) is required for antimalarial induced apoptosis. Despite inhibiting autophagy, neither CQ treatment nor RNAi against autophagy regulators (ATGs) promote cell death. In contrast, Q triggers high levels of apoptosis, both in vitro and in vivo, and this phenotype requires both autophagy inhibition and p53-dependent inhibition of the oxPPP. Simultaneous genetic targeting of the oxPPP and autophagy is sufficient to trigger apoptosis in lung cancer cells, including cells lacking p53. Thus, in addition to reduced autophagy, oxPPP inhibition serves as an important determinant of antimalarial cytotoxicity in cancer cells.
DOI: 10.1038/onc.2015.348
PubMed: 26434592
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000230
Links to Exploration step
pubmed:26434592Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.</title><author><name sortKey="Salas, E" sort="Salas, E" uniqKey="Salas E" first="E" last="Salas">E. Salas</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Roy, S" sort="Roy, S" uniqKey="Roy S" first="S" last="Roy">S. Roy</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Marsh, T" sort="Marsh, T" uniqKey="Marsh T" first="T" last="Marsh">T. Marsh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Rubin, B" sort="Rubin, B" uniqKey="Rubin B" first="B" last="Rubin">B. Rubin</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Anatomic Pathology and Molecular Genetics, Cleveland Clinic, Cleveland, OH, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Anatomic Pathology and Molecular Genetics, Cleveland Clinic, Cleveland, OH</wicri:regionArea></affiliation></author><author><name sortKey="Debnath, J" sort="Debnath, J" uniqKey="Debnath J" first="J" last="Debnath">J. Debnath</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26434592</idno><idno type="pmid">26434592</idno><idno type="doi">10.1038/onc.2015.348</idno><idno type="wicri:Area/PubMed/Corpus">000230</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000230</idno><idno type="wicri:Area/PubMed/Curation">000230</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000230</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.</title><author><name sortKey="Salas, E" sort="Salas, E" uniqKey="Salas E" first="E" last="Salas">E. Salas</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Roy, S" sort="Roy, S" uniqKey="Roy S" first="S" last="Roy">S. Roy</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Marsh, T" sort="Marsh, T" uniqKey="Marsh T" first="T" last="Marsh">T. Marsh</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author><author><name sortKey="Rubin, B" sort="Rubin, B" uniqKey="Rubin B" first="B" last="Rubin">B. Rubin</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Anatomic Pathology and Molecular Genetics, Cleveland Clinic, Cleveland, OH, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Anatomic Pathology and Molecular Genetics, Cleveland Clinic, Cleveland, OH</wicri:regionArea></affiliation></author><author><name sortKey="Debnath, J" sort="Debnath, J" uniqKey="Debnath J" first="J" last="Debnath">J. Debnath</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA</wicri:regionArea></affiliation></author></analytic><series><title level="j">Oncogene</title><idno type="eISSN">1476-5594</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antimalarials (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (pharmacology)</term><term>Humans</term><term>Lung Neoplasms (pathology)</term><term>Mutation</term><term>Oxidation-Reduction (drug effects)</term><term>Pentose Phosphate Pathway (drug effects)</term><term>Proto-Oncogene Proteins p21(ras) (genetics)</term><term>Tumor Suppressor Protein p53 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antipaludiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mutation</term><term>Oxydoréduction ()</term><term>Prolifération cellulaire ()</term><term>Protéine p53 suppresseur de tumeur (métabolisme)</term><term>Protéines proto-oncogènes p21(ras) (génétique)</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Voie des pentoses phosphates ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Proto-Oncogene Proteins p21(ras)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antimalarials</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><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>Oxidation-Reduction</term><term>Pentose Phosphate Pathway</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines proto-oncogènes p21(ras)</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéine p53 suppresseur de tumeur</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antipaludiques</term><term>Chloroquine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term><term>Mutation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mutation</term><term>Oxydoréduction</term><term>Prolifération cellulaire</term><term>Voie des pentoses phosphates</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite immense interest in using antimalarials as autophagy inhibitors to treat cancer, it remains unclear whether these agents act predominantly via autophagy inhibition or whether other pathways direct their anti-cancer properties. By comparing the treatment effects of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demonstrate that inhibition of the oxidative arm of the pentose phosphate pathway (oxPPP) is required for antimalarial induced apoptosis. Despite inhibiting autophagy, neither CQ treatment nor RNAi against autophagy regulators (ATGs) promote cell death. In contrast, Q triggers high levels of apoptosis, both in vitro and in vivo, and this phenotype requires both autophagy inhibition and p53-dependent inhibition of the oxPPP. Simultaneous genetic targeting of the oxPPP and autophagy is sufficient to trigger apoptosis in lung cancer cells, including cells lacking p53. Thus, in addition to reduced autophagy, oxPPP inhibition serves as an important determinant of antimalarial cytotoxicity in cancer cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26434592</PMID><DateCompleted><Year>2017</Year><Month>08</Month><Day>28</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5594</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>22</Issue><PubDate><Year>2016</Year><Month>06</Month><Day>02</Day></PubDate></JournalIssue><Title>Oncogene</Title><ISOAbbreviation>Oncogene</ISOAbbreviation></Journal><ArticleTitle>Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.</ArticleTitle><Pagination><MedlinePgn>2913-22</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/onc.2015.348</ELocationID><Abstract><AbstractText>Despite immense interest in using antimalarials as autophagy inhibitors to treat cancer, it remains unclear whether these agents act predominantly via autophagy inhibition or whether other pathways direct their anti-cancer properties. By comparing the treatment effects of the antimalarials chloroquine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demonstrate that inhibition of the oxidative arm of the pentose phosphate pathway (oxPPP) is required for antimalarial induced apoptosis. Despite inhibiting autophagy, neither CQ treatment nor RNAi against autophagy regulators (ATGs) promote cell death. In contrast, Q triggers high levels of apoptosis, both in vitro and in vivo, and this phenotype requires both autophagy inhibition and p53-dependent inhibition of the oxPPP. Simultaneous genetic targeting of the oxPPP and autophagy is sufficient to trigger apoptosis in lung cancer cells, including cells lacking p53. Thus, in addition to reduced autophagy, oxPPP inhibition serves as an important determinant of antimalarial cytotoxicity in cancer cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Salas</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roy</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marsh</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rubin</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Departments of Anatomic Pathology and Molecular Genetics, Cleveland Clinic, Cleveland, OH, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Debnath</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA126792</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA188404</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>10</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Oncogene</MedlineTA><NlmUniqueID>8711562</NlmUniqueID><ISSNLinking>0950-9232</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000962">Antimalarials</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C117307">KRAS protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016159">Tumor Suppressor Protein p53</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.6.5.2</RegistryNumber><NameOfSubstance UI="D016283">Proto-Oncogene Proteins p21(ras)</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000962" MajorTopicYN="N">Antimalarials</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">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="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</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="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010427" MajorTopicYN="N">Pentose Phosphate Pathway</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016283" MajorTopicYN="N">Proto-Oncogene Proteins p21(ras)</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016159" MajorTopicYN="N">Tumor Suppressor Protein p53</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>01</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>07</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>08</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>10</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>10</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>8</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26434592</ArticleId><ArticleId IdType="pii">onc2015348</ArticleId><ArticleId IdType="doi">10.1038/onc.2015.348</ArticleId><ArticleId IdType="pmc">PMC4821829</ArticleId><ArticleId IdType="mid">NIHMS716603</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cancer Discov. 2014 Apr;4(4):466-79</Citation><ArticleIdList><ArticleId IdType="pubmed">24513958</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2008 Jan;118(1):79-88</Citation><ArticleIdList><ArticleId IdType="pubmed">18097482</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14333-8</Citation><ArticleIdList><ArticleId IdType="pubmed">20660757</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10 (8):1369-79</Citation><ArticleIdList><ArticleId IdType="pubmed">24991839</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2009 Sep 3;461(7260):109-13</Citation><ArticleIdList><ArticleId IdType="pubmed">19693011</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2003 Jan 30;421(6922):499-506</Citation><ArticleIdList><ArticleId IdType="pubmed">12556884</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Mol Cell Biol. 2010 Oct;11(10):715-27</Citation><ArticleIdList><ArticleId IdType="pubmed">20861880</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Commun Signal. 2011 May 15;9:13</Citation><ArticleIdList><ArticleId IdType="pubmed">21569639</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2013 Dec 12;504(7479):296-300</Citation><ArticleIdList><ArticleId IdType="pubmed">24305049</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Pathol. 2013 Jan 24;8:105-37</Citation><ArticleIdList><ArticleId IdType="pubmed">23072311</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Biol Ther. 2011 Aug 1;12 (3):239-51</Citation><ArticleIdList><ArticleId IdType="pubmed">21725213</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10(8):1415-25</Citation><ArticleIdList><ArticleId IdType="pubmed">24991836</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2011 Oct 1;25(19):1999-2010</Citation><ArticleIdList><ArticleId IdType="pubmed">21979913</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10(8):1403-14</Citation><ArticleIdList><ArticleId IdType="pubmed">24991835</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Cancer Res. 2011 Feb 15;17(4):654-66</Citation><ArticleIdList><ArticleId IdType="pubmed">21325294</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2011 Apr 1;25(7):717-29</Citation><ArticleIdList><ArticleId IdType="pubmed">21406549</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuro Oncol. 2010 May;12(5):473-81</Citation><ArticleIdList><ArticleId IdType="pubmed">20406898</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10(8):1380-90</Citation><ArticleIdList><ArticleId IdType="pubmed">24991834</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Res. 2014 May 1;74(9):2579-90</Citation><ArticleIdList><ArticleId IdType="pubmed">24590058</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Discov. 2014 Aug;4(8):905-13</Citation><ArticleIdList><ArticleId IdType="pubmed">24875860</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2011 Mar 1;25(5):460-70</Citation><ArticleIdList><ArticleId IdType="pubmed">21317241</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2013 Jul 1;27(13):1447-61</Citation><ArticleIdList><ArticleId IdType="pubmed">23824538</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Cell. 2014 Aug 11;26(2):190-206</Citation><ArticleIdList><ArticleId IdType="pubmed">25117709</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2012 Apr;8(4):445-544</Citation><ArticleIdList><ArticleId IdType="pubmed">22966490</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2008 Mar;19(3):797-806</Citation><ArticleIdList><ArticleId IdType="pubmed">18094039</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Cell Biol. 2011 Mar;13(3):310-6</Citation><ArticleIdList><ArticleId IdType="pubmed">21336310</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2012 Feb 1;8(2):200-12</Citation><ArticleIdList><ArticleId IdType="pubmed">22252008</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2005 Nov 29;102(48):17448-53</Citation><ArticleIdList><ArticleId IdType="pubmed">16287968</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncologist. 2014 Jun;19(6):637-8</Citation><ArticleIdList><ArticleId IdType="pubmed">24821822</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10 (8):1359-68</Citation><ArticleIdList><ArticleId IdType="pubmed">24991840</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Cancer. 2009 Oct;9(10):691-700</Citation><ArticleIdList><ArticleId IdType="pubmed">19759539</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2014 Aug;10(8):1391-402</Citation><ArticleIdList><ArticleId IdType="pubmed">24991838</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Cell. 2011 Jan 15;22(2):165-78</Citation><ArticleIdList><ArticleId IdType="pubmed">21119005</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2012 May 22;109 (21):8253-8</Citation><ArticleIdList><ArticleId IdType="pubmed">22566612</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Discov. 2014 Aug;4(8):914-27</Citation><ArticleIdList><ArticleId IdType="pubmed">24875857</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000230 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000230 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:26434592
|texte= Oxidative pentose phosphate pathway inhibition is a key determinant of antimalarial induced cancer cell death.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:26434592" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |