Tetrandrine Increases the Sensitivity of Human Lung Adenocarcinoma PC14 Cells to Gefitinib by Lysosomal Inhibition.
Identifieur interne : 000C93 ( Ncbi/Merge ); précédent : 000C92; suivant : 000C94Tetrandrine Increases the Sensitivity of Human Lung Adenocarcinoma PC14 Cells to Gefitinib by Lysosomal Inhibition.
Auteurs : Eiko Sato [Japon] ; Sinya Ohta [Japon] ; Kenjiro Kawakami [Japon] ; Mana Ikeda [Japon] ; Tatsuo Takahashi [Japon] ; Shinjiro Kobayashi [Japon] ; Masaaki Nomura [Japon]Source :
- Anticancer research [ 1791-7530 ] ; 2019.
Descripteurs français
- KwdFr :
- Autophagie, Benzylisoquinoléines (), Benzylisoquinoléines (pharmacologie), Humains, Lignée cellulaire tumorale, Lysosomes (), Lysosomes (métabolisme), Prolifération cellulaire (), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Récepteurs ErbB (génétique), Régulation de l'expression des gènes tumoraux (), Résistance aux médicaments antinéoplasiques (), Survie cellulaire (), Synergie des médicaments, Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- génétique : Protéines associées aux microtubules, Récepteurs ErbB, Tumeurs du poumon.
- métabolisme : Lysosomes, Protéines associées aux microtubules, Tumeurs du poumon.
- pharmacologie : Benzylisoquinoléines.
- traitement médicamenteux : Tumeurs du poumon.
- Autophagie, Benzylisoquinoléines, Humains, Lignée cellulaire tumorale, Lysosomes, Prolifération cellulaire, Régulation de l'expression des gènes tumoraux, Résistance aux médicaments antinéoplasiques, Survie cellulaire, Synergie des médicaments.
English descriptors
- KwdEn :
- Adenocarcinoma of Lung (drug therapy), Adenocarcinoma of Lung (genetics), Adenocarcinoma of Lung (metabolism), Autophagy, Benzylisoquinolines (chemistry), Benzylisoquinolines (pharmacology), Cell Line, Tumor, Cell Proliferation (drug effects), Cell Survival (drug effects), Drug Resistance, Neoplasm (drug effects), Drug Synergism, ErbB Receptors (genetics), Gefitinib (chemistry), Gefitinib (pharmacology), Gene Expression Regulation, Neoplastic (drug effects), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lysosomes (drug effects), Lysosomes (metabolism), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism).
- MESH :
- chemical , chemistry : Benzylisoquinolines, Gefitinib.
- drug effects : Cell Proliferation, Cell Survival, Drug Resistance, Neoplasm, Gene Expression Regulation, Neoplastic, Lysosomes.
- drug therapy : Adenocarcinoma of Lung, Lung Neoplasms.
- genetics : Adenocarcinoma of Lung, ErbB Receptors, Lung Neoplasms, Microtubule-Associated Proteins.
- metabolism : Adenocarcinoma of Lung, Lung Neoplasms, Lysosomes, Microtubule-Associated Proteins.
- chemical , pharmacology : Benzylisoquinolines, Gefitinib.
- Autophagy, Cell Line, Tumor, Drug Synergism, Humans.
Abstract
Human lung adenocarcinoma PC14 cells without mutations in the epidermal growth factor receptor (EGFR) are less sensitive to gefitinib than PC9 cells with EGFR mutations. We report the involvement of tetrandrine in autophagy flux as a mechanism that enhances the sensitivity of PC14 cells to gefitinib.
DOI: 10.21873/anticanres.13874
PubMed: 31810924
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000016
- to stream PubMed, to step Curation: 000016
- to stream PubMed, to step Checkpoint: 000023
Links to Exploration step
pubmed:31810924Le document en format XML
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type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma of Lung (drug therapy)</term><term>Adenocarcinoma of Lung (genetics)</term><term>Adenocarcinoma of Lung (metabolism)</term><term>Autophagy</term><term>Benzylisoquinolines (chemistry)</term><term>Benzylisoquinolines (pharmacology)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Drug Resistance, Neoplasm (drug effects)</term><term>Drug Synergism</term><term>ErbB Receptors (genetics)</term><term>Gefitinib (chemistry)</term><term>Gefitinib (pharmacology)</term><term>Gene Expression Regulation, Neoplastic (drug effects)</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (metabolism)</term><term>Lysosomes (drug effects)</term><term>Lysosomes (metabolism)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie</term><term>Benzylisoquinoléines ()</term><term>Benzylisoquinoléines (pharmacologie)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Lysosomes ()</term><term>Lysosomes (métabolisme)</term><term>Prolifération cellulaire ()</term><term>Protéines associées aux microtubules (génétique)</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Récepteurs ErbB (génétique)</term><term>Régulation de l'expression des gènes tumoraux ()</term><term>Résistance aux médicaments antinéoplasiques ()</term><term>Survie cellulaire ()</term><term>Synergie des médicaments</term><term>Tumeurs du poumon (génétique)</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Benzylisoquinolines</term><term>Gefitinib</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term><term>Cell Survival</term><term>Drug Resistance, Neoplasm</term><term>Gene Expression Regulation, Neoplastic</term><term>Lysosomes</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>ErbB Receptors</term><term>Lung Neoplasms</term><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines associées aux microtubules</term><term>Récepteurs ErbB</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Lung Neoplasms</term><term>Lysosomes</term><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Lysosomes</term><term>Protéines associées aux microtubules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Benzylisoquinoléines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzylisoquinolines</term><term>Gefitinib</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autophagy</term><term>Cell Line, Tumor</term><term>Drug Synergism</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Benzylisoquinoléines</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Lysosomes</term><term>Prolifération cellulaire</term><term>Régulation de l'expression des gènes tumoraux</term><term>Résistance aux médicaments antinéoplasiques</term><term>Survie cellulaire</term><term>Synergie des médicaments</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Human lung adenocarcinoma PC14 cells without mutations in the epidermal growth factor receptor (EGFR) are less sensitive to gefitinib than PC9 cells with EGFR mutations. We report the involvement of tetrandrine in autophagy flux as a mechanism that enhances the sensitivity of PC14 cells to gefitinib.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31810924</PMID><DateCompleted><Year>2019</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2020</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1791-7530</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>12</Issue><PubDate><Year>2019</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Anticancer research</Title><ISOAbbreviation>Anticancer Res.</ISOAbbreviation></Journal><ArticleTitle>Tetrandrine Increases the Sensitivity of Human Lung Adenocarcinoma PC14 Cells to Gefitinib by Lysosomal Inhibition.</ArticleTitle><Pagination><MedlinePgn>6585-6593</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.21873/anticanres.13874</ELocationID><Abstract><AbstractText Label="BACKGROUND/AIM" NlmCategory="OBJECTIVE">Human lung adenocarcinoma PC14 cells without mutations in the epidermal growth factor receptor (EGFR) are less sensitive to gefitinib than PC9 cells with EGFR mutations. We report the involvement of tetrandrine in autophagy flux as a mechanism that enhances the sensitivity of PC14 cells to gefitinib.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">Sensitivity to gefitinib was determined by a growth inhibition assay, and quantitative real-time PCR, western blotting, and fluorescent immunostaining were used to detect autophagy.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In PC14 cells, combined treatment with gefitinib and tetrandrine caused a significant increase in gefitinib sensitivity and autophagy-related mRNAs and proteins (LC3, etc.), and the LC3 protein accumulated in lysosomes. Furthermore, an autophagy flux assay revealed that tetrandrine inhibited lysosomes and that gefitinib promoted autophagy. Finally, the sensitivity of PC14 cells to gefitinib was enhanced with chloroquine.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Tetrandrine possibly increases the susceptibility of PC14 cells to gefitinib by lysosomal inhibition.</AbstractText><CopyrightInformation>Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sato</LastName><ForeName>Eiko</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ohta</LastName><ForeName>Sinya</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kawakami</LastName><ForeName>Kenjiro</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ikeda</LastName><ForeName>Mana</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takahashi</LastName><ForeName>Tatsuo</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kobayashi</LastName><ForeName>Shinjiro</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nomura</LastName><ForeName>Masaaki</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan m-nomura@hokuriku-u.ac.jp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Anticancer Res</MedlineTA><NlmUniqueID>8102988</NlmUniqueID><ISSNLinking>0250-7005</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D044182">Benzylisoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C466626">light chain 3, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>29EX23D5AJ</RegistryNumber><NameOfSubstance UI="C009438">tetrandrine</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><Chemical><RegistryNumber>S65743JHBS</RegistryNumber><NameOfSubstance UI="D000077156">Gefitinib</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000077192" MajorTopicYN="N">Adenocarcinoma of Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044182" MajorTopicYN="N">Benzylisoquinolines</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</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="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077156" MajorTopicYN="N">Gefitinib</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></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="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Human lung adenocarcinoma PC14 cells</Keyword><Keyword MajorTopicYN="N">autophagy flux</Keyword><Keyword MajorTopicYN="N">gefitinib</Keyword><Keyword MajorTopicYN="N">lysosomal inhibition</Keyword><Keyword MajorTopicYN="N">tetrandrine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>10</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>12</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31810924</ArticleId><ArticleId IdType="pii">39/12/6585</ArticleId><ArticleId IdType="doi">10.21873/anticanres.13874</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Sato, Eiko" sort="Sato, Eiko" uniqKey="Sato E" first="Eiko" last="Sato">Eiko Sato</name></noRegion><name sortKey="Ikeda, Mana" sort="Ikeda, Mana" uniqKey="Ikeda M" first="Mana" last="Ikeda">Mana Ikeda</name><name sortKey="Kawakami, Kenjiro" sort="Kawakami, Kenjiro" uniqKey="Kawakami K" first="Kenjiro" last="Kawakami">Kenjiro Kawakami</name><name sortKey="Kobayashi, Shinjiro" sort="Kobayashi, Shinjiro" uniqKey="Kobayashi S" first="Shinjiro" last="Kobayashi">Shinjiro Kobayashi</name><name sortKey="Nomura, Masaaki" sort="Nomura, Masaaki" uniqKey="Nomura M" first="Masaaki" last="Nomura">Masaaki Nomura</name><name sortKey="Ohta, Sinya" sort="Ohta, Sinya" uniqKey="Ohta S" first="Sinya" last="Ohta">Sinya Ohta</name><name sortKey="Takahashi, Tatsuo" sort="Takahashi, Tatsuo" uniqKey="Takahashi T" first="Tatsuo" last="Takahashi">Tatsuo Takahashi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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