Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.
Identifieur interne : 000063 ( PubMed/Curation ); précédent : 000062; suivant : 000064Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.
Auteurs : Satabdi Datta [Inde] ; Diptiman Choudhury [Inde] ; Amlan Das [Inde] ; Dipanwita Das Mukherjee [Inde] ; Moumita Dasgupta [Inde] ; Shreya Bandopadhyay [Inde] ; Gopal Chakrabarti [Inde]Source :
- Apoptosis : an international journal on programmed cell death [ 1573-675X ] ; 2019.
Abstract
Paclitaxel is one of the most commonly used drugs for the treatment of nonsmall cell lung cancer (NSCLC). However acquired resistance to paclitaxel, epithelial to mesenchymal transition and cancer stem cell formation are the major obstacles for successful chemotherapy with this drug. Some of the major reasons behind chemoresistance development include increased ability of the cancer cells to survive under stress conditions by autophagy, increased expression of drug efflux pumps, tubulin mutations etc. In this study we found that inhibition of autophagy with chloroquine prevented development of paclitaxel resistance in A549 cells with time and potentiated the effect of paclitaxel by increased accumulation of superoxide-producing damaged mitochondria, with elevated ROS generation, it also increased the apoptotic rate and sub G0/ G1 phase arrest with time in A549 cells treated with paclitaxel and attenuated the metastatic potential and cancer stem cell population of the paclitaxel-resistant cells by ROS mediated modulation of the Wnt/β-catenin signaling pathway, thereby increasing paclitaxel sensitivity. ROS here played a crucial role in modulating Akt activity when autophagy process was hindered by chloroquine, excessive ROS accumulation in the cell inhibited Akt activity. In addition, chloroquine pre-treatment followed by taxol (10 nM) treatment did not show significant toxicity towards non-carcinomas WI38 cells (lung fibroblast cells). Thus autophagy inhibition by CQ pre-treatment can be used as a fruitful strategy to combat the phenomenon of paclitaxel resistance development as well as metastasis in lung cancer.
DOI: 10.1007/s10495-019-01526-y
PubMed: 30767087
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000063
Links to Exploration step
pubmed:30767087Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.</title>
<author><name sortKey="Datta, Satabdi" sort="Datta, Satabdi" uniqKey="Datta S" first="Satabdi" last="Datta">Satabdi Datta</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Choudhury, Diptiman" sort="Choudhury, Diptiman" uniqKey="Choudhury D" first="Diptiman" last="Choudhury">Diptiman Choudhury</name>
<affiliation wicri:level="1"><nlm:affiliation>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Das, Amlan" sort="Das, Amlan" uniqKey="Das A" first="Amlan" last="Das">Amlan Das</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Mukherjee, Dipanwita Das" sort="Mukherjee, Dipanwita Das" uniqKey="Mukherjee D" first="Dipanwita Das" last="Mukherjee">Dipanwita Das Mukherjee</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Dasgupta, Moumita" sort="Dasgupta, Moumita" uniqKey="Dasgupta M" first="Moumita" last="Dasgupta">Moumita Dasgupta</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Bandopadhyay, Shreya" sort="Bandopadhyay, Shreya" uniqKey="Bandopadhyay S" first="Shreya" last="Bandopadhyay">Shreya Bandopadhyay</name>
<affiliation wicri:level="1"><nlm:affiliation>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chakrabarti, Gopal" sort="Chakrabarti, Gopal" uniqKey="Chakrabarti G" first="Gopal" last="Chakrabarti">Gopal Chakrabarti</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India. gcbcg@caluniv.ac.in.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2019">2019</date>
<idno type="RBID">pubmed:30767087</idno>
<idno type="pmid">30767087</idno>
<idno type="doi">10.1007/s10495-019-01526-y</idno>
<idno type="wicri:Area/PubMed/Corpus">000063</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000063</idno>
<idno type="wicri:Area/PubMed/Curation">000063</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000063</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.</title>
<author><name sortKey="Datta, Satabdi" sort="Datta, Satabdi" uniqKey="Datta S" first="Satabdi" last="Datta">Satabdi Datta</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Choudhury, Diptiman" sort="Choudhury, Diptiman" uniqKey="Choudhury D" first="Diptiman" last="Choudhury">Diptiman Choudhury</name>
<affiliation wicri:level="1"><nlm:affiliation>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Das, Amlan" sort="Das, Amlan" uniqKey="Das A" first="Amlan" last="Das">Amlan Das</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Mukherjee, Dipanwita Das" sort="Mukherjee, Dipanwita Das" uniqKey="Mukherjee D" first="Dipanwita Das" last="Mukherjee">Dipanwita Das Mukherjee</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Dasgupta, Moumita" sort="Dasgupta, Moumita" uniqKey="Dasgupta M" first="Moumita" last="Dasgupta">Moumita Dasgupta</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Bandopadhyay, Shreya" sort="Bandopadhyay, Shreya" uniqKey="Bandopadhyay S" first="Shreya" last="Bandopadhyay">Shreya Bandopadhyay</name>
<affiliation wicri:level="1"><nlm:affiliation>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032, India.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chakrabarti, Gopal" sort="Chakrabarti, Gopal" uniqKey="Chakrabarti G" first="Gopal" last="Chakrabarti">Gopal Chakrabarti</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India. gcbcg@caluniv.ac.in.</nlm:affiliation>
<country xml:lang="fr">Inde</country>
<wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Apoptosis : an international journal on programmed cell death</title>
<idno type="eISSN">1573-675X</idno>
<imprint><date when="2019" type="published">2019</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Paclitaxel is one of the most commonly used drugs for the treatment of nonsmall cell lung cancer (NSCLC). However acquired resistance to paclitaxel, epithelial to mesenchymal transition and cancer stem cell formation are the major obstacles for successful chemotherapy with this drug. Some of the major reasons behind chemoresistance development include increased ability of the cancer cells to survive under stress conditions by autophagy, increased expression of drug efflux pumps, tubulin mutations etc. In this study we found that inhibition of autophagy with chloroquine prevented development of paclitaxel resistance in A549 cells with time and potentiated the effect of paclitaxel by increased accumulation of superoxide-producing damaged mitochondria, with elevated ROS generation, it also increased the apoptotic rate and sub G0/ G1 phase arrest with time in A549 cells treated with paclitaxel and attenuated the metastatic potential and cancer stem cell population of the paclitaxel-resistant cells by ROS mediated modulation of the Wnt/β-catenin signaling pathway, thereby increasing paclitaxel sensitivity. ROS here played a crucial role in modulating Akt activity when autophagy process was hindered by chloroquine, excessive ROS accumulation in the cell inhibited Akt activity. In addition, chloroquine pre-treatment followed by taxol (10 nM) treatment did not show significant toxicity towards non-carcinomas WI38 cells (lung fibroblast cells). Thus autophagy inhibition by CQ pre-treatment can be used as a fruitful strategy to combat the phenomenon of paclitaxel resistance development as well as metastasis in lung cancer.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">30767087</PMID>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>26</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-675X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>24</Volume>
<Issue>5-6</Issue>
<PubDate><Year>2019</Year>
<Month>06</Month>
</PubDate>
</JournalIssue>
<Title>Apoptosis : an international journal on programmed cell death</Title>
<ISOAbbreviation>Apoptosis</ISOAbbreviation>
</Journal>
<ArticleTitle>Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.</ArticleTitle>
<Pagination><MedlinePgn>414-433</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s10495-019-01526-y</ELocationID>
<Abstract><AbstractText>Paclitaxel is one of the most commonly used drugs for the treatment of nonsmall cell lung cancer (NSCLC). However acquired resistance to paclitaxel, epithelial to mesenchymal transition and cancer stem cell formation are the major obstacles for successful chemotherapy with this drug. Some of the major reasons behind chemoresistance development include increased ability of the cancer cells to survive under stress conditions by autophagy, increased expression of drug efflux pumps, tubulin mutations etc. In this study we found that inhibition of autophagy with chloroquine prevented development of paclitaxel resistance in A549 cells with time and potentiated the effect of paclitaxel by increased accumulation of superoxide-producing damaged mitochondria, with elevated ROS generation, it also increased the apoptotic rate and sub G0/ G1 phase arrest with time in A549 cells treated with paclitaxel and attenuated the metastatic potential and cancer stem cell population of the paclitaxel-resistant cells by ROS mediated modulation of the Wnt/β-catenin signaling pathway, thereby increasing paclitaxel sensitivity. ROS here played a crucial role in modulating Akt activity when autophagy process was hindered by chloroquine, excessive ROS accumulation in the cell inhibited Akt activity. In addition, chloroquine pre-treatment followed by taxol (10 nM) treatment did not show significant toxicity towards non-carcinomas WI38 cells (lung fibroblast cells). Thus autophagy inhibition by CQ pre-treatment can be used as a fruitful strategy to combat the phenomenon of paclitaxel resistance development as well as metastasis in lung cancer.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Datta</LastName>
<ForeName>Satabdi</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Choudhury</LastName>
<ForeName>Diptiman</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Das</LastName>
<ForeName>Amlan</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mukherjee</LastName>
<ForeName>Dipanwita Das</ForeName>
<Initials>DD</Initials>
<AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dasgupta</LastName>
<ForeName>Moumita</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bandopadhyay</LastName>
<ForeName>Shreya</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chakrabarti</LastName>
<ForeName>Gopal</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India. gcbcg@caluniv.ac.in.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>. SR/SO/BB-14/2008 and BT/ PR12889/AGR/36/624/2009</GrantID>
<Agency>Department of Science and Technology, Government of India(IN) and Department of Biotechnology, Govt of India</Agency>
<Country>International</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Apoptosis</MedlineTA>
<NlmUniqueID>9712129</NlmUniqueID>
<ISSNLinking>1360-8185</ISSNLinking>
</MedlineJournalInfo>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Apoptosis. 2019 Mar 28;:</RefSource>
<PMID Version="1">30923989</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword>
<Keyword MajorTopicYN="Y">Chloroquine</Keyword>
<Keyword MajorTopicYN="Y">EMT</Keyword>
<Keyword MajorTopicYN="Y">Paclitaxel-resistance</Keyword>
<Keyword MajorTopicYN="Y">ROS</Keyword>
<Keyword MajorTopicYN="Y">β-Catenin</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year>
<Month>2</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>2</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2019</Year>
<Month>2</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">30767087</ArticleId>
<ArticleId IdType="doi">10.1007/s10495-019-01526-y</ArticleId>
<ArticleId IdType="pii">10.1007/s10495-019-01526-y</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000063 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000063 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= ChloroquineV1 |flux= PubMed |étape= Curation |type= RBID |clé= pubmed:30767087 |texte= Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:30767087" \ | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \ | NlmPubMed2Wicri -a ChloroquineV1
![]() | This area was generated with Dilib version V0.6.33. | ![]() |