[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].
Identifieur interne : 000131 ( PubMed/Curation ); précédent : 000130; suivant : 000132[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].
Auteurs : Yaping Zhang [République populaire de Chine] ; Li Cao [République populaire de Chine] ; Qiang Su [République populaire de Chine] ; Kai Cheng [République populaire de Chine] ; Xiaoyan Zhang [Oman]Source :
- Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology [ 1007-8738 ] ; 2017.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Apoptose (), Autophagie (), Camptothécine (pharmacologie), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Chloroquine (pharmacologie), Facteur de croissance transformant bêta-1 (analyse), Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- analogues et dérivés : Adénine.
- analyse : Facteur de croissance transformant bêta-1.
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- pharmacologie : Adénine, Camptothécine, Chloroquine.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Prolifération cellulaire.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Camptothecin (pharmacology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Transforming Growth Factor beta1 (analysis).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , analysis : Transforming Growth Factor beta1.
- chemical , pharmacology : Adenine, Camptothecin, Chloroquine.
- drug effects : Apoptosis, Autophagy, Cell Proliferation.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Humans.
Abstract
Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.
PubMed: 29382424
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Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001</wicri:regionArea></affiliation></author><author><name sortKey="Su, Qiang" sort="Su, Qiang" uniqKey="Su Q" first="Qiang" last="Su">Qiang Su</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Neurology, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Neurology, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001</wicri:regionArea></affiliation></author><author><name sortKey="Cheng, Kai" sort="Cheng, Kai" uniqKey="Cheng K" first="Kai" last="Cheng">Kai Cheng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Xiaoyan" sort="Zhang, Xiaoyan" uniqKey="Zhang X" first="Xiaoyan" last="Zhang">Xiaoyan Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author, E-mail: 931326464@qq.com.</nlm:affiliation><country wicri:rule="url">Oman</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:29382424</idno><idno type="pmid">29382424</idno><idno type="wicri:Area/PubMed/Corpus">000131</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000131</idno><idno type="wicri:Area/PubMed/Curation">000131</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000131</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].</title><author><name sortKey="Zhang, Yaping" sort="Zhang, Yaping" uniqKey="Zhang Y" first="Yaping" last="Zhang">Yaping Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001</wicri:regionArea></affiliation></author><author><name sortKey="Cao, Li" sort="Cao, Li" uniqKey="Cao L" first="Li" last="Cao">Li Cao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001</wicri:regionArea></affiliation></author><author><name sortKey="Su, Qiang" sort="Su, Qiang" uniqKey="Su Q" first="Qiang" last="Su">Qiang Su</name><affiliation wicri:level="1"><nlm:affiliation>Key Laboratory of Neurology, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Laboratory of Neurology, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001</wicri:regionArea></affiliation></author><author><name sortKey="Cheng, Kai" sort="Cheng, Kai" uniqKey="Cheng K" first="Kai" last="Cheng">Kai Cheng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Xiaoyan" sort="Zhang, Xiaoyan" uniqKey="Zhang X" first="Xiaoyan" last="Zhang">Xiaoyan Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author, E-mail: 931326464@qq.com.</nlm:affiliation><country wicri:rule="url">Oman</country><wicri:regionArea>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author</wicri:regionArea></affiliation></author></analytic><series><title level="j">Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology</title><idno type="ISSN">1007-8738</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Camptothecin (pharmacology)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</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 (drug therapy)</term><term>Lung Neoplasms (pathology)</term><term>Transforming Growth Factor beta1 (analysis)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénine (analogues et dérivés)</term><term>Adénine (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Camptothécine (pharmacologie)</term><term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Chloroquine (pharmacologie)</term><term>Facteur de croissance transformant bêta-1 (analyse)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire ()</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Transforming Growth Factor beta1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Camptothecin</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adénine</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Facteur de croissance transformant bêta-1</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></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="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>Adénine</term><term>Camptothécine</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Prolifération cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29382424</PMID><DateCompleted><Year>2018</Year><Month>08</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>08</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1007-8738</ISSN><JournalIssue CitedMedium="Print"><Volume>33</Volume><Issue>12</Issue><PubDate><Year>2017</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology</Title><ISOAbbreviation>Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi</ISOAbbreviation></Journal><ArticleTitle>[Inhibition of autophagy initiation stage enhances camptothecin-induced apoptosis in NCI-H1975 cells].</ArticleTitle><Pagination><MedlinePgn>1640-1646</MedlinePgn></Pagination><Abstract><AbstractText>Objective To explore the effect of autophagic inhibitors chloroquine (CQ) and 3-methyl adenine (3-MA) on apoptosis of non-small cell lung adenocarcinoma NCI-H1975 cells induced by camptothecin (CPT). Methods After NCI-H1975 cells were treated with CPT, cell proliferation was detected by CCK-8 assay, morphological changes of cells were observed by PI staining, and the apoptosis of NCI-H1975 cells was determined by flow cytometry. The levels of autophagy-and apoptosis-related proteins LC3I, LC3II, P62, caspase-3 and poly ADP-ribose polymerase (PARP) and transforming growth factor beta 1 (TGF-beta 1) were detected by Western blot analysis. Results After CPT treatment, the ratio of LC3II to LC3I was raised. The apoptotic protease caspase-3 and substrate PARP were obviously degraded, which could be enhanced by 3-MA but inhibited by CQ. It was also found that the intracellular TGF-beta 1 was reduced after CPT treatment. Conclusion Inhibition of autophagy initiation stage in NCI-H1975 cells can increase the sensitivity of cell apoptosis induced by CPT.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yaping</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Qiang</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Key Laboratory of Neurology, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Kai</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xiaoyan</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Medical Laboratory Science, Fenyang College of Shanxi Medical University, Fenyang 032200; Shanxi Medical University, First Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China. *Corresponding author, E-mail: 931326464@qq.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>chi</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>China</Country><MedlineTA>Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi</MedlineTA><NlmUniqueID>101139110</NlmUniqueID><ISSNLinking>1007-8738</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053773">Transforming Growth Factor beta1</NameOfSubstance></Chemical><Chemical><RegistryNumber>5142-23-4</RegistryNumber><NameOfSubstance UI="C025946">3-methyladenine</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>JAC85A2161</RegistryNumber><NameOfSubstance UI="D000225">Adenine</NameOfSubstance></Chemical><Chemical><RegistryNumber>XT3Z54Z28A</RegistryNumber><NameOfSubstance UI="D002166">Camptothecin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000225" MajorTopicYN="N">Adenine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><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="D002166" MajorTopicYN="N">Camptothecin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</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="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="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053773" MajorTopicYN="N">Transforming Growth Factor beta1</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>8</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29382424</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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