Inhibition of autophagy by chloroquine potentiates synergistically anti-cancer property of artemisinin by promoting ROS dependent apoptosis.
Identifieur interne : 000281 ( PubMed/Curation ); précédent : 000280; suivant : 000282Inhibition of autophagy by chloroquine potentiates synergistically anti-cancer property of artemisinin by promoting ROS dependent apoptosis.
Auteurs : Arnab Ganguli [Inde] ; Diptiman Choudhury [Inde] ; Satabdi Datta [Inde] ; Surela Bhattacharya [Inde] ; Gopal Chakrabarti [Inde]Source :
- Biochimie [ 1638-6183 ] ; 2014.
Descripteurs français
- KwdFr :
- Apoptose (), Apoptose (physiologie), Artémisinines (administration et posologie), Artémisinines (pharmacologie), Autophagie (), Chloroquine (administration et posologie), Chloroquine (pharmacologie), Cycle cellulaire (), Espèces réactives de l'oxygène (métabolisme), Humains, Lignée cellulaire tumorale (), Potentiel de membrane mitochondriale (), Protocoles de polychimiothérapie antinéoplasique (pharmacologie), Survie cellulaire (), Synergie des médicaments.
- MESH :
- administration et posologie : Artémisinines, Chloroquine.
- métabolisme : Espèces réactives de l'oxygène.
- pharmacologie : Artémisinines, Chloroquine, Protocoles de polychimiothérapie antinéoplasique.
- physiologie : Apoptose.
- Apoptose, Autophagie, Cycle cellulaire, Humains, Lignée cellulaire tumorale, Potentiel de membrane mitochondriale, Survie cellulaire, Synergie des médicaments.
English descriptors
- KwdEn :
- Antineoplastic Combined Chemotherapy Protocols (pharmacology), Apoptosis (drug effects), Apoptosis (physiology), Artemisinins (administration & dosage), Artemisinins (pharmacology), Autophagy (drug effects), Cell Cycle (drug effects), Cell Line, Tumor (drug effects), Cell Survival (drug effects), Chloroquine (administration & dosage), Chloroquine (pharmacology), Drug Synergism, Humans, Membrane Potential, Mitochondrial (drug effects), Reactive Oxygen Species (metabolism).
- MESH :
- chemical , administration & dosage : Artemisinins, Chloroquine.
- drug effects : Apoptosis, Autophagy, Cell Cycle, Cell Line, Tumor, Cell Survival, Membrane Potential, Mitochondrial.
- chemical , metabolism : Reactive Oxygen Species.
- pharmacology : Antineoplastic Combined Chemotherapy Protocols, Artemisinins, Chloroquine.
- physiology : Apoptosis.
- Drug Synergism, Humans.
Abstract
Artemisinin (ART) is a well-known anti-malarial drug, and recently it is shown prospective to selectively kill cancer cells. But low potency makes it inappropriate for use as an anticancer drug. In this study, we modulated the ART-induced autophagy to increase Potency of ART as an anticancer agent. ART reduced the cell viability and colony forming ability of non-small lung carcinoma (A549) cells and it was non-toxic against normal lung (WI38) cells. ART induced autophagy at the early stage of treatment. Pre-treatment with chloroquine (CQ) and followed by ART treatment had synergistic combination index (CI) for cell death. Inhibition of autophagy by CQ pre-treatment led to accumulation of acidic vacuoles (AVOs) which acquainted with unprocessed damage mitochondria that subsequently promoted ROS generation, and resulted releases of Cyt C in cytosol that caused caspase-3 dependent apoptosis cell death in ART-treated A549 cells. Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis. Similar effects were observed in other cancer cells SCC25 and MDA-MB-231. The appropriate manipulation of autophagy by using CQ provides a powerful strategy to increase the Potency of selective anticancer property of ART.
DOI: 10.1016/j.biochi.2014.10.001
PubMed: 25308836
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Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB 700019</wicri:regionArea></affiliation></author></analytic><series><title level="j">Biochimie</title><idno type="eISSN">1638-6183</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Combined Chemotherapy Protocols (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Apoptosis (physiology)</term><term>Artemisinins (administration & dosage)</term><term>Artemisinins (pharmacology)</term><term>Autophagy (drug effects)</term><term>Cell Cycle (drug effects)</term><term>Cell Line, Tumor (drug effects)</term><term>Cell Survival (drug effects)</term><term>Chloroquine (administration & dosage)</term><term>Chloroquine (pharmacology)</term><term>Drug Synergism</term><term>Humans</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Reactive Oxygen Species (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose ()</term><term>Apoptose (physiologie)</term><term>Artémisinines (administration et posologie)</term><term>Artémisinines (pharmacologie)</term><term>Autophagie ()</term><term>Chloroquine (administration et posologie)</term><term>Chloroquine (pharmacologie)</term><term>Cycle cellulaire ()</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lignée cellulaire tumorale ()</term><term>Potentiel de membrane mitochondriale ()</term><term>Protocoles de polychimiothérapie antinéoplasique (pharmacologie)</term><term>Survie cellulaire ()</term><term>Synergie des médicaments</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Artemisinins</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Artémisinines</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Cycle</term><term>Cell Line, Tumor</term><term>Cell Survival</term><term>Membrane Potential, Mitochondrial</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Artémisinines</term><term>Chloroquine</term><term>Protocoles de polychimiothérapie antinéoplasique</term></keywords><keywords scheme="MESH" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Combined Chemotherapy Protocols</term><term>Artemisinins</term><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Drug Synergism</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Cycle cellulaire</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Potentiel de membrane mitochondriale</term><term>Survie cellulaire</term><term>Synergie des médicaments</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Artemisinin (ART) is a well-known anti-malarial drug, and recently it is shown prospective to selectively kill cancer cells. But low potency makes it inappropriate for use as an anticancer drug. In this study, we modulated the ART-induced autophagy to increase Potency of ART as an anticancer agent. ART reduced the cell viability and colony forming ability of non-small lung carcinoma (A549) cells and it was non-toxic against normal lung (WI38) cells. ART induced autophagy at the early stage of treatment. Pre-treatment with chloroquine (CQ) and followed by ART treatment had synergistic combination index (CI) for cell death. Inhibition of autophagy by CQ pre-treatment led to accumulation of acidic vacuoles (AVOs) which acquainted with unprocessed damage mitochondria that subsequently promoted ROS generation, and resulted releases of Cyt C in cytosol that caused caspase-3 dependent apoptosis cell death in ART-treated A549 cells. Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis. Similar effects were observed in other cancer cells SCC25 and MDA-MB-231. The appropriate manipulation of autophagy by using CQ provides a powerful strategy to increase the Potency of selective anticancer property of ART. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25308836</PMID><DateCompleted><Year>2015</Year><Month>08</Month><Day>06</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1638-6183</ISSN><JournalIssue CitedMedium="Internet"><Volume>107 Pt B</Volume><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Biochimie</Title><ISOAbbreviation>Biochimie</ISOAbbreviation></Journal><ArticleTitle>Inhibition of autophagy by chloroquine potentiates synergistically anti-cancer property of artemisinin by promoting ROS dependent apoptosis.</ArticleTitle><Pagination><MedlinePgn>338-49</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biochi.2014.10.001</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0300-9084(14)00287-9</ELocationID><Abstract><AbstractText>Artemisinin (ART) is a well-known anti-malarial drug, and recently it is shown prospective to selectively kill cancer cells. But low potency makes it inappropriate for use as an anticancer drug. In this study, we modulated the ART-induced autophagy to increase Potency of ART as an anticancer agent. ART reduced the cell viability and colony forming ability of non-small lung carcinoma (A549) cells and it was non-toxic against normal lung (WI38) cells. ART induced autophagy at the early stage of treatment. Pre-treatment with chloroquine (CQ) and followed by ART treatment had synergistic combination index (CI) for cell death. Inhibition of autophagy by CQ pre-treatment led to accumulation of acidic vacuoles (AVOs) which acquainted with unprocessed damage mitochondria that subsequently promoted ROS generation, and resulted releases of Cyt C in cytosol that caused caspase-3 dependent apoptosis cell death in ART-treated A549 cells. Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis. Similar effects were observed in other cancer cells SCC25 and MDA-MB-231. The appropriate manipulation of autophagy by using CQ provides a powerful strategy to increase the Potency of selective anticancer property of ART. </AbstractText><CopyrightInformation>Copyright © 2014 Elsevier B.V. and Société française de biochimie et biologie Moléculaire (SFBBM). All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ganguli</LastName><ForeName>Arnab</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB 700019, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choudhury</LastName><ForeName>Diptiman</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB 700019, India.</Affiliation></AffiliationInfo></Author><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, Kolkata, WB 700019, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bhattacharya</LastName><ForeName>Surela</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, Kolkata, WB 700019, 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, Kolkata, WB 700019, India. Electronic address: gcbcg@caluniv.ac.in.</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>2014</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Biochimie</MedlineTA><NlmUniqueID>1264604</NlmUniqueID><ISSNLinking>0300-9084</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D037621">Artemisinins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9RMU91N5K2</RegistryNumber><NameOfSubstance UI="C031327">artemisinine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000971" MajorTopicYN="N">Antineoplastic Combined Chemotherapy Protocols</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D037621" MajorTopicYN="N">Artemisinins</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><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="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</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="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053078" MajorTopicYN="N">Membrane Potential, Mitochondrial</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Anticancer agent</Keyword><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Artemisinin</Keyword><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">Chloroquine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>07</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>10</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>8</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25308836</ArticleId><ArticleId IdType="pii">S0300-9084(14)00287-9</ArticleId><ArticleId IdType="doi">10.1016/j.biochi.2014.10.001</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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