ChloroquineV1, PubMed, Curation, bibRecord, 000303

Induction of autophagy contributes to crizotinib resistance in ALK-positive lung cancer.

Identifieur interne : 000303 ( PubMed/Curation ); précédent : 000302; suivant : 000304

Induction of autophagy contributes to crizotinib resistance in ALK-positive lung cancer.

Auteurs : Cheng Ji [République populaire de Chine] ; Li Zhang [États-Unis] ; Yan Cheng [États-Unis] ; Raj Patel [États-Unis] ; Hao Wu [États-Unis] ; Yi Zhang [États-Unis] ; Mian Wang [États-Unis] ; Shundong Ji [États-Unis] ; Chandra P. Belani [États-Unis] ; Jin-Ming Yang [États-Unis] ; Xingcong Ren [États-Unis]

Source :

Cancer biology & therapy [ 1555-8576 ] ; 2014.

RBID : pubmed:24556908

Descripteurs français

KwdFr :
- Animaux, Antinéoplasiques (pharmacologie), Autophagie (), Chloroquine (pharmacologie), Femelle, Humains, Hétérogreffes, Lignée cellulaire tumorale, Pyrazoles (pharmacologie), Pyridines (pharmacologie), Récepteurs à activité tyrosine kinase (génétique), Récepteurs à activité tyrosine kinase (métabolisme), Régulation négative, Résistance aux médicaments antinéoplasiques (), Souris nude, Sérine-thréonine kinases TOR (métabolisme), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
MESH :
- anatomopathologie : Tumeurs du poumon.
- génétique : Récepteurs à activité tyrosine kinase.
- métabolisme : Récepteurs à activité tyrosine kinase, Sérine-thréonine kinases TOR.
- pharmacologie : Antinéoplasiques, Chloroquine, Pyrazoles, Pyridines.
- traitement médicamenteux : Tumeurs du poumon.
- Animaux, Autophagie, Femelle, Humains, Hétérogreffes, Lignée cellulaire tumorale, Régulation négative, Résistance aux médicaments antinéoplasiques, Souris nude.

English descriptors

KwdEn :
- Anaplastic Lymphoma Kinase, Animals, Antineoplastic Agents (pharmacology), Autophagy (drug effects), Cell Line, Tumor, Chloroquine (pharmacology), Crizotinib, Down-Regulation, Drug Resistance, Neoplasm (drug effects), Female, Heterografts, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Mice, Nude, Pyrazoles (pharmacology), Pyridines (pharmacology), Receptor Protein-Tyrosine Kinases (genetics), Receptor Protein-Tyrosine Kinases (metabolism), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , genetics : Receptor Protein-Tyrosine Kinases.
- chemical , metabolism : Receptor Protein-Tyrosine Kinases, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Antineoplastic Agents, Chloroquine, Pyrazoles, Pyridines.
- chemical : Anaplastic Lymphoma Kinase, Crizotinib.
- drug effects : Autophagy, Drug Resistance, Neoplasm.
- drug therapy : Lung Neoplasms.
- pathology : Lung Neoplasms.
- Animals, Cell Line, Tumor, Down-Regulation, Female, Heterografts, Humans, Mice, Nude.

Abstract

Use of the inhibitor of ALK fusion onco-protein, crizotinib (PF02341066), has achieved impressive clinical efficacy in patients with ALK-positive non-small cell lung cancer. Nevertheless, acquired resistance to this drug occurs inevitably in approximately a year, limiting the therapeutic benefits of this novel targeted therapy. In this study, we found that autophagy was induced in crizonitib-resistant lung cancer cells and contributed to drug resistance. We observed that ALK was downregulated in the crizotinib-resistant lung cancer cell line, H3122CR-1, and this was causally associated with autophagy induction. The degree of crizotinib resistance correlated with autophagic activity. Activation of autophagy in crizotinib-resistant H3122CR-1 cells involved alteration of the Akt/mTOR signaling pathway. Furthermore, we demonstrated that chloroquine, an inhibitor of autophagy, could restore sensitivity of H3122CR-1 to crizotinib and enhance its efficacy against drug-resistant lung cancer. Thus, modulating autophagy may be worth exploring as a new strategy to overcome acquired crizonitib resistance in ALK-positive lung cancer.

DOI: 10.4161/cbt.28162
PubMed: 24556908

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<term>Chloroquine (pharmacology)</term>
<term>Crizotinib</term>
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<term>Antinéoplasiques (pharmacologie)</term>
<term>Autophagie ()</term>
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<term>Autophagie</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hétérogreffes</term>
<term>Lignée cellulaire tumorale</term>
<term>Régulation négative</term>
<term>Résistance aux médicaments antinéoplasiques</term>
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<front><div type="abstract" xml:lang="en">Use of the inhibitor of ALK fusion onco-protein, crizotinib (PF02341066), has achieved impressive clinical efficacy in patients with ALK-positive non-small cell lung cancer. Nevertheless, acquired resistance to this drug occurs inevitably in approximately a year, limiting the therapeutic benefits of this novel targeted therapy. In this study, we found that autophagy was induced in crizonitib-resistant lung cancer cells and contributed to drug resistance. We observed that ALK was downregulated in the crizotinib-resistant lung cancer cell line, H3122CR-1, and this was causally associated with autophagy induction. The degree of crizotinib resistance correlated with autophagic activity. Activation of autophagy in crizotinib-resistant H3122CR-1 cells involved alteration of the Akt/mTOR signaling pathway. Furthermore, we demonstrated that chloroquine, an inhibitor of autophagy, could restore sensitivity of H3122CR-1 to crizotinib and enhance its efficacy against drug-resistant lung cancer. Thus, modulating autophagy may be worth exploring as a new strategy to overcome acquired crizonitib resistance in ALK-positive lung cancer. </div>
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<Title>Cancer biology & therapy</Title>
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<ArticleTitle>Induction of autophagy contributes to crizotinib resistance in ALK-positive lung cancer.</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.4161/cbt.28162</ELocationID>
<Abstract><AbstractText>Use of the inhibitor of ALK fusion onco-protein, crizotinib (PF02341066), has achieved impressive clinical efficacy in patients with ALK-positive non-small cell lung cancer. Nevertheless, acquired resistance to this drug occurs inevitably in approximately a year, limiting the therapeutic benefits of this novel targeted therapy. In this study, we found that autophagy was induced in crizonitib-resistant lung cancer cells and contributed to drug resistance. We observed that ALK was downregulated in the crizotinib-resistant lung cancer cell line, H3122CR-1, and this was causally associated with autophagy induction. The degree of crizotinib resistance correlated with autophagic activity. Activation of autophagy in crizotinib-resistant H3122CR-1 cells involved alteration of the Akt/mTOR signaling pathway. Furthermore, we demonstrated that chloroquine, an inhibitor of autophagy, could restore sensitivity of H3122CR-1 to crizotinib and enhance its efficacy against drug-resistant lung cancer. Thus, modulating autophagy may be worth exploring as a new strategy to overcome acquired crizonitib resistance in ALK-positive lung cancer. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ji</LastName>
<ForeName>Cheng</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA; Department of Respiratory Medicine; The First Affiliated Hospital of Soochow University; Suzhou, Jiangsu, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Li</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Patel</LastName>
<ForeName>Raj</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Hao</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Mian</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ji</LastName>
<ForeName>Shundong</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Belani</LastName>
<ForeName>Chandra P</ForeName>
<Initials>CP</Initials>
<AffiliationInfo><Affiliation>Department of Medicine; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Jin-Ming</ForeName>
<Initials>JM</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Xingcong</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology; Penn State Hershey Cancer Institute; The Pennsylvania State University College of Medicine and Milton S. Hershey Medical Center; Hershey, PA USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>02</Month>
<Day>20</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Cancer Biol Ther</MedlineTA>
<NlmUniqueID>101137842</NlmUniqueID>
<ISSNLinking>1538-4047</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011720">Pyrazoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011725">Pyridines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>53AH36668S</RegistryNumber>
<NameOfSubstance UI="D000077547">Crizotinib</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>886U3H6UFF</RegistryNumber>
<NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="C000626173">ALK protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="C000626174">Alk protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D000077548">Anaplastic Lymphoma Kinase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D020794">Receptor Protein-Tyrosine Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000077548" MajorTopicYN="N">Anaplastic Lymphoma Kinase</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug 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="D000077547" MajorTopicYN="N">Crizotinib</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D064593" MajorTopicYN="N">Heterografts</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="Q000473" MajorTopicYN="Y">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
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<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ALK</Keyword>
<Keyword MajorTopicYN="N">autophagy</Keyword>
<Keyword MajorTopicYN="N">crizotinib</Keyword>
<Keyword MajorTopicYN="N">drug resistance</Keyword>
<Keyword MajorTopicYN="N">lung cancer</Keyword>
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Induction of autophagy contributes to crizotinib resistance in ALK-positive lung cancer.

Induction of autophagy contributes to crizotinib resistance in ALK-positive lung cancer.

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