ChloroquineV1, PubMed, Checkpoint, bibRecord, 000245

Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

Identifieur interne : 000245 ( PubMed/Checkpoint ); précédent : 000244; suivant : 000246

Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

Source :

Oncotarget [ 1949-2553 ] ; 2015.

RBID : pubmed:26384345

Descripteurs français

English descriptors

KwdEn :
- Animals, Autophagy (drug effects), Cell Line, Tumor, Cell Survival (drug effects), Crizotinib, Drug Synergism, Eukaryotic Initiation Factor-2 (metabolism), Female, Humans, Hydroxychloroquine (pharmacology), Immunoblotting, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Mice, Inbred BALB C, Mice, Nude, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Microtubule-Associated Proteins (metabolism), Phagosomes (drug effects), Phagosomes (metabolism), Phagosomes (ultrastructure), Phosphorylation (drug effects), Proto-Oncogene Proteins c-bcl-2 (metabolism), Pyrazoles (pharmacology), Pyridines (pharmacology), STAT3 Transcription Factor (metabolism), Signal Transduction (drug effects), Xenograft Model Antitumor Assays.
MESH :
- chemical , metabolism : Eukaryotic Initiation Factor-2, Microtubule-Associated Proteins, Proto-Oncogene Proteins c-bcl-2, STAT3 Transcription Factor.
- chemical , pharmacology : Hydroxychloroquine, Pyrazoles, Pyridines.
- chemical : Crizotinib.
- drug effects : Autophagy, Cell Survival, Phagosomes, Phosphorylation, Signal Transduction.
- drug therapy : Lung Neoplasms.
- metabolism : Lung Neoplasms, Phagosomes.
- ultrastructure : Phagosomes.
- Animals, Cell Line, Tumor, Drug Synergism, Female, Humans, Immunoblotting, Mice, Inbred BALB C, Mice, Nude, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Xenograft Model Antitumor Assays.

Abstract

Autophagy is an evolutionarily conserved survival pathway in eukaryote and is frequently upregulated in cancer cells after chemotherapy or targeted therapy. Thus induction of autophagy has emerged as a drug resistance mechanism. In this study, we found that crizotinib induced a high level of autophagy in lung cancer cells through inhibition of STAT3. Ectopic expression of wild-type or constitutive activated STAT3 significantly suppressed the effect of crizotinib on autophagy. Interestingly, crizotinib-mediated inhibition of STAT3 is in a step-wise manner. Firstly it inhibited cytoplasmic STAT3, which leads to the phosphorylation of EIF2A, then inhibited nuclear STAT3, which leads to the downregulation of BCL-2. Cell death induced by crizotinib was greatly enhanced after the inhibition of autophagy by the pharmacological inhibitors or shRNAs against Beclin-1. Moreover, the autophagy inhibitor HCQ significantly augmented the anti-tumor effect of crizotinib in a mouse xenograft model. In conclusion, crizotinib can induce cytoprotective autophagy by suppression of STAT3 in lung cancer cells. Thus, autophagy inhibition represents a promising approach to improve the efficacy of crizotinib in the treatment of targeted lung cancer patients.

DOI: 10.18632/oncotarget.5592
PubMed: 26384345

Affiliations:

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<author><name sortKey="Yao, Junlin" sort="Yao, Junlin" uniqKey="Yao J" first="Junlin" last="Yao">Junlin Yao</name>
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<author><name sortKey="Li, Hongsen" sort="Li, Hongsen" uniqKey="Li H" first="Hongsen" last="Li">Hongsen Li</name>
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<author><name sortKey="Xie, Jiansheng" sort="Xie, Jiansheng" uniqKey="Xie J" first="Jiansheng" last="Xie">Jiansheng Xie</name>
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<author><name sortKey="Wang, Zhanggui" sort="Wang, Zhanggui" uniqKey="Wang Z" first="Zhanggui" last="Wang">Zhanggui Wang</name>
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<author><name sortKey="Huang, Wendong" sort="Huang, Wendong" uniqKey="Huang W" first="Wendong" last="Huang">Wendong Huang</name>
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<author><name sortKey="Han, Weidong" sort="Han, Weidong" uniqKey="Han W" first="Weidong" last="Han">Weidong Han</name>
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<author><name sortKey="Shou, Jiawei" sort="Shou, Jiawei" uniqKey="Shou J" first="Jiawei" last="Shou">Jiawei Shou</name>
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<author><name sortKey="Jing, Zhao" sort="Jing, Zhao" uniqKey="Jing Z" first="Zhao" last="Jing">Zhao Jing</name>
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<author><name sortKey="Yao, Junlin" sort="Yao, Junlin" uniqKey="Yao J" first="Junlin" last="Yao">Junlin Yao</name>
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<placeName><settlement type="city">Hangzhou</settlement>
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</placeName>
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<author><name sortKey="Li, Hongsen" sort="Li, Hongsen" uniqKey="Li H" first="Hongsen" last="Li">Hongsen Li</name>
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<author><name sortKey="Xie, Jiansheng" sort="Xie, Jiansheng" uniqKey="Xie J" first="Jiansheng" last="Xie">Jiansheng Xie</name>
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<author><name sortKey="Wang, Zhanggui" sort="Wang, Zhanggui" uniqKey="Wang Z" first="Zhanggui" last="Wang">Zhanggui Wang</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<orgName type="university">Université de Zhejiang</orgName>
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<author><name sortKey="Pan, Qin" sort="Pan, Qin" uniqKey="Pan Q" first="Qin" last="Pan">Qin Pan</name>
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<author><name sortKey="Huang, Wendong" sort="Huang, Wendong" uniqKey="Huang W" first="Wendong" last="Huang">Wendong Huang</name>
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<author><name sortKey="Han, Weidong" sort="Han, Weidong" uniqKey="Han W" first="Weidong" last="Han">Weidong Han</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Autophagy (drug effects)</term>
<term>Cell Line, Tumor</term>
<term>Cell Survival (drug effects)</term>
<term>Crizotinib</term>
<term>Drug Synergism</term>
<term>Eukaryotic Initiation Factor-2 (metabolism)</term>
<term>Female</term>
<term>Humans</term>
<term>Hydroxychloroquine (pharmacology)</term>
<term>Immunoblotting</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Microscopy, Electron, Transmission</term>
<term>Microscopy, Fluorescence</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Phagosomes (drug effects)</term>
<term>Phagosomes (metabolism)</term>
<term>Phagosomes (ultrastructure)</term>
<term>Phosphorylation (drug effects)</term>
<term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term>
<term>Pyrazoles (pharmacology)</term>
<term>Pyridines (pharmacology)</term>
<term>STAT3 Transcription Factor (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Autophagie ()</term>
<term>Facteur de transcription STAT-3 (métabolisme)</term>
<term>Facteur-2 d'initiation eucaryote (métabolisme)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hydroxychloroquine (pharmacologie)</term>
<term>Immunotransfert</term>
<term>Lignée cellulaire tumorale</term>
<term>Microscopie de fluorescence</term>
<term>Microscopie électronique à transmission</term>
<term>Phagosomes ()</term>
<term>Phagosomes (métabolisme)</term>
<term>Phagosomes (ultrastructure)</term>
<term>Phosphorylation ()</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term>
<term>Pyrazoles (pharmacologie)</term>
<term>Pyridines (pharmacologie)</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
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<term>Synergie des médicaments</term>
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<term>Tumeurs du poumon (traitement médicamenteux)</term>
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<term>Drug Synergism</term>
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<term>Humans</term>
<term>Immunoblotting</term>
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<term>Mice, Nude</term>
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<term>Microscopy, Fluorescence</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Humains</term>
<term>Immunotransfert</term>
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<front><div type="abstract" xml:lang="en">Autophagy is an evolutionarily conserved survival pathway in eukaryote and is frequently upregulated in cancer cells after chemotherapy or targeted therapy. Thus induction of autophagy has emerged as a drug resistance mechanism. In this study, we found that crizotinib induced a high level of autophagy in lung cancer cells through inhibition of STAT3. Ectopic expression of wild-type or constitutive activated STAT3 significantly suppressed the effect of crizotinib on autophagy. Interestingly, crizotinib-mediated inhibition of STAT3 is in a step-wise manner. Firstly it inhibited cytoplasmic STAT3, which leads to the phosphorylation of EIF2A, then inhibited nuclear STAT3, which leads to the downregulation of BCL-2. Cell death induced by crizotinib was greatly enhanced after the inhibition of autophagy by the pharmacological inhibitors or shRNAs against Beclin-1. Moreover, the autophagy inhibitor HCQ significantly augmented the anti-tumor effect of crizotinib in a mouse xenograft model. In conclusion, crizotinib can induce cytoprotective autophagy by suppression of STAT3 in lung cancer cells. Thus, autophagy inhibition represents a promising approach to improve the efficacy of crizotinib in the treatment of targeted lung cancer patients. </div>
</front>
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<DateCompleted><Year>2016</Year>
<Month>09</Month>
<Day>20</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>12</Month>
<Day>02</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>6</Volume>
<Issue>37</Issue>
<PubDate><Year>2015</Year>
<Month>Nov</Month>
<Day>24</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.</ArticleTitle>
<Pagination><MedlinePgn>40268-82</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.5592</ELocationID>
<Abstract><AbstractText>Autophagy is an evolutionarily conserved survival pathway in eukaryote and is frequently upregulated in cancer cells after chemotherapy or targeted therapy. Thus induction of autophagy has emerged as a drug resistance mechanism. In this study, we found that crizotinib induced a high level of autophagy in lung cancer cells through inhibition of STAT3. Ectopic expression of wild-type or constitutive activated STAT3 significantly suppressed the effect of crizotinib on autophagy. Interestingly, crizotinib-mediated inhibition of STAT3 is in a step-wise manner. Firstly it inhibited cytoplasmic STAT3, which leads to the phosphorylation of EIF2A, then inhibited nuclear STAT3, which leads to the downregulation of BCL-2. Cell death induced by crizotinib was greatly enhanced after the inhibition of autophagy by the pharmacological inhibitors or shRNAs against Beclin-1. Moreover, the autophagy inhibitor HCQ significantly augmented the anti-tumor effect of crizotinib in a mouse xenograft model. In conclusion, crizotinib can induce cytoprotective autophagy by suppression of STAT3 in lung cancer cells. Thus, autophagy inhibition represents a promising approach to improve the efficacy of crizotinib in the treatment of targeted lung cancer patients. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>You</LastName>
<ForeName>Liangkun</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shou</LastName>
<ForeName>Jiawei</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Deng</LastName>
<ForeName>Danchen</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Gynaecology and Obstetrics, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Liming</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jing</LastName>
<ForeName>Zhao</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yao</LastName>
<ForeName>Junlin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Hongsen</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xie</LastName>
<ForeName>Jiansheng</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Zhanggui</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pan</LastName>
<ForeName>Qin</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pan</LastName>
<ForeName>Hongming</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Wendong</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Division of Molecular Diabetes Research, Department of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Han</LastName>
<ForeName>Weidong</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ISSNLinking>1949-2553</ISSNLinking>
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</MeshHeading>
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</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Zhejiang</li>
</region>
<settlement><li>Hangzhou</li>
</settlement>
<orgName><li>Université de Zhejiang</li>
</orgName>
</list>
<tree><country name="République populaire de Chine"><region name="Zhejiang"><name sortKey="You, Liangkun" sort="You, Liangkun" uniqKey="You L" first="Liangkun" last="You">Liangkun You</name>
</region>
<name sortKey="Deng, Danchen" sort="Deng, Danchen" uniqKey="Deng D" first="Danchen" last="Deng">Danchen Deng</name>
<name sortKey="Han, Weidong" sort="Han, Weidong" uniqKey="Han W" first="Weidong" last="Han">Weidong Han</name>
<name sortKey="Jiang, Liming" sort="Jiang, Liming" uniqKey="Jiang L" first="Liming" last="Jiang">Liming Jiang</name>
<name sortKey="Jing, Zhao" sort="Jing, Zhao" uniqKey="Jing Z" first="Zhao" last="Jing">Zhao Jing</name>
<name sortKey="Li, Hongsen" sort="Li, Hongsen" uniqKey="Li H" first="Hongsen" last="Li">Hongsen Li</name>
<name sortKey="Pan, Hongming" sort="Pan, Hongming" uniqKey="Pan H" first="Hongming" last="Pan">Hongming Pan</name>
<name sortKey="Pan, Qin" sort="Pan, Qin" uniqKey="Pan Q" first="Qin" last="Pan">Qin Pan</name>
<name sortKey="Shou, Jiawei" sort="Shou, Jiawei" uniqKey="Shou J" first="Jiawei" last="Shou">Jiawei Shou</name>
<name sortKey="Wang, Zhanggui" sort="Wang, Zhanggui" uniqKey="Wang Z" first="Zhanggui" last="Wang">Zhanggui Wang</name>
<name sortKey="Xie, Jiansheng" sort="Xie, Jiansheng" uniqKey="Xie J" first="Jiansheng" last="Xie">Jiansheng Xie</name>
<name sortKey="Yao, Junlin" sort="Yao, Junlin" uniqKey="Yao J" first="Junlin" last="Yao">Junlin Yao</name>
</country>
<country name="États-Unis"><region name="Californie"><name sortKey="Huang, Wendong" sort="Huang, Wendong" uniqKey="Huang W" first="Wendong" last="Huang">Wendong Huang</name>
</region>
</country>
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Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

Crizotinib induces autophagy through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

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