Inhibition of autophagy by chloroquine potentiates synergistically anti-cancer property of artemisinin by promoting ROS dependent apoptosis.
Identifieur interne : 001017 ( Main/Exploration ); précédent : 001016; suivant : 001018Inhibition 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
Affiliations:
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Le document en format XML
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Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB 700019, 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, Kolkata, WB 700019</wicri:regionArea><wicri:noRegion>WB 700019</wicri:noRegion></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>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.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Biotechnology and Dr. B.C. 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Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB 700019</wicri:regionArea><wicri:noRegion>WB 700019</wicri:noRegion></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, Kolkata, WB 700019, India. Electronic address: 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, Kolkata, WB 700019</wicri:regionArea><wicri:noRegion>WB 700019</wicri:noRegion></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><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Ganguli, Arnab" sort="Ganguli, Arnab" uniqKey="Ganguli A" first="Arnab" last="Ganguli">Arnab Ganguli</name></noRegion><name sortKey="Bhattacharya, Surela" sort="Bhattacharya, Surela" uniqKey="Bhattacharya S" first="Surela" last="Bhattacharya">Surela Bhattacharya</name><name sortKey="Chakrabarti, Gopal" sort="Chakrabarti, Gopal" uniqKey="Chakrabarti G" first="Gopal" last="Chakrabarti">Gopal Chakrabarti</name><name sortKey="Choudhury, Diptiman" sort="Choudhury, Diptiman" uniqKey="Choudhury D" first="Diptiman" last="Choudhury">Diptiman Choudhury</name><name sortKey="Datta, Satabdi" sort="Datta, Satabdi" uniqKey="Datta S" first="Satabdi" last="Datta">Satabdi Datta</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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