Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.
Identifieur interne : 000059 ( PubMed/Corpus ); précédent : 000058; suivant : 000060Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.
Auteurs : Li Li ; Yubo Wang ; Lin Jiao ; Caiyu Lin ; Conghua Lu ; Kejun Zhang ; Chen Hu ; Junyi Ye ; Dadong Zhang ; Haiyan Wu ; Mingxia Feng ; Yong HeSource :
- Cancer letters [ 1872-7980 ] ; 2019.
English descriptors
- KwdEn :
- Acrylamides (pharmacology), Aldehyde Dehydrogenase 1 (biosynthesis), Aniline Compounds (pharmacology), Animals, Antineoplastic Agents (pharmacology), Autophagy (drug effects), Beclin-1 (genetics), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Chloroquine (pharmacology), Drug Resistance, Neoplasm (genetics), ErbB Receptors (genetics), Female, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Mice, Mice, Inbred BALB C, Protein Kinase Inhibitors (pharmacology), RNA Interference, RNA, Small Interfering (genetics), Retinal Dehydrogenase (biosynthesis), SOXB1 Transcription Factors (biosynthesis), Xenograft Model Antitumor Assays.
- MESH :
- chemical , biosynthesis : Aldehyde Dehydrogenase 1, Retinal Dehydrogenase, SOXB1 Transcription Factors.
- chemical , genetics : Beclin-1, ErbB Receptors, RNA, Small Interfering.
- chemical , pharmacology : Acrylamides, Aniline Compounds, Antineoplastic Agents, Chloroquine, Protein Kinase Inhibitors.
- drug effects : Autophagy.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Drug Resistance, Neoplasm.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Animals, Cell Line, Tumor, Female, Humans, Mice, Mice, Inbred BALB C, RNA Interference, Xenograft Model Antitumor Assays.
Abstract
Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.
DOI: 10.1016/j.canlet.2019.03.027
PubMed: 30910592
Links to Exploration step
pubmed:30910592Le document en format XML
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Electronic address: heyong8998@126.com.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:30910592</idno><idno type="pmid">30910592</idno><idno type="doi">10.1016/j.canlet.2019.03.027</idno><idno type="wicri:Area/PubMed/Corpus">000059</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000059</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.</title><author><name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yubo" sort="Wang, Yubo" uniqKey="Wang Y" first="Yubo" last="Wang">Yubo Wang</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Jiao, Lin" sort="Jiao, Lin" uniqKey="Jiao L" first="Lin" last="Jiao">Lin Jiao</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Lin, Caiyu" sort="Lin, Caiyu" uniqKey="Lin C" first="Caiyu" last="Lin">Caiyu Lin</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, Conghua" sort="Lu, Conghua" uniqKey="Lu C" first="Conghua" last="Lu">Conghua Lu</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Kejun" sort="Zhang, Kejun" uniqKey="Zhang K" first="Kejun" last="Zhang">Kejun Zhang</name><affiliation><nlm:affiliation>Department of Clinical Laboratory, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Hu, Chen" sort="Hu, Chen" uniqKey="Hu C" first="Chen" last="Hu">Chen Hu</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ye, Junyi" sort="Ye, Junyi" uniqKey="Ye J" first="Junyi" last="Ye">Junyi Ye</name><affiliation><nlm:affiliation>Burning Rock Biotech, Guangzhou, 510300, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Dadong" sort="Zhang, Dadong" uniqKey="Zhang D" first="Dadong" last="Zhang">Dadong Zhang</name><affiliation><nlm:affiliation>The Research and Development Institute of Precision Medicine, 3D Medicine Inc., Shanghai, 201114, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wu, Haiyan" sort="Wu, Haiyan" uniqKey="Wu H" first="Haiyan" last="Wu">Haiyan Wu</name><affiliation><nlm:affiliation>OrigiMed Co. Ltd, Shanghai, 201114, China.</nlm:affiliation></affiliation></author><author><name sortKey="Feng, Mingxia" sort="Feng, Mingxia" uniqKey="Feng M" first="Mingxia" last="Feng">Mingxia Feng</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</nlm:affiliation></affiliation></author><author><name sortKey="He, Yong" sort="He, Yong" uniqKey="He Y" first="Yong" last="He">Yong He</name><affiliation><nlm:affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China. Electronic address: heyong8998@126.com.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cancer letters</title><idno type="eISSN">1872-7980</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acrylamides (pharmacology)</term><term>Aldehyde Dehydrogenase 1 (biosynthesis)</term><term>Aniline Compounds (pharmacology)</term><term>Animals</term><term>Antineoplastic Agents (pharmacology)</term><term>Autophagy (drug effects)</term><term>Beclin-1 (genetics)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>Drug Resistance, Neoplasm (genetics)</term><term>ErbB Receptors (genetics)</term><term>Female</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (pathology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Protein Kinase Inhibitors (pharmacology)</term><term>RNA Interference</term><term>RNA, Small Interfering (genetics)</term><term>Retinal Dehydrogenase (biosynthesis)</term><term>SOXB1 Transcription Factors (biosynthesis)</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Aldehyde Dehydrogenase 1</term><term>Retinal Dehydrogenase</term><term>SOXB1 Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Beclin-1</term><term>ErbB Receptors</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Acrylamides</term><term>Aniline Compounds</term><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Protein Kinase Inhibitors</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</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="genetics" xml:lang="en"><term>Drug Resistance, Neoplasm</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" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Female</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>RNA Interference</term><term>Xenograft Model Antitumor Assays</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30910592</PMID><DateCompleted><Year>2020</Year><Month>02</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7980</ISSN><JournalIssue CitedMedium="Internet"><Volume>452</Volume><PubDate><Year>2019</Year><Month>06</Month><Day>28</Day></PubDate></JournalIssue><Title>Cancer letters</Title><ISOAbbreviation>Cancer Lett.</ISOAbbreviation></Journal><ArticleTitle>Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.</ArticleTitle><Pagination><MedlinePgn>191-202</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0304-3835(19)30183-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.canlet.2019.03.027</ELocationID><Abstract><AbstractText>Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Yubo</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiao</LastName><ForeName>Lin</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Caiyu</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Conghua</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Kejun</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ye</LastName><ForeName>Junyi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Burning Rock Biotech, Guangzhou, 510300, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Dadong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>The Research and Development Institute of Precision Medicine, 3D Medicine Inc., Shanghai, 201114, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Haiyan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>OrigiMed Co. Ltd, Shanghai, 201114, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Mingxia</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Yong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, 400042, China. Electronic address: heyong8998@126.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>03</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Cancer Lett</MedlineTA><NlmUniqueID>7600053</NlmUniqueID><ISSNLinking>0304-3835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000178">Acrylamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000080924">Aldehyde Dehydrogenase 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000814">Aniline 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UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.2.1.36</RegistryNumber><NameOfSubstance UI="C510223">ALDH1A1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.2.1.36</RegistryNumber><NameOfSubstance UI="D050697">Retinal Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="C512478">EGFR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D066246">ErbB Receptors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000178" MajorTopicYN="N">Acrylamides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000080924" MajorTopicYN="N">Aldehyde Dehydrogenase 1</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000814" MajorTopicYN="N">Aniline Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></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="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</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="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D047428" MajorTopicYN="N">Protein Kinase Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050697" MajorTopicYN="N">Retinal Dehydrogenase</DescriptorName><QualifierName 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