Chloroquine inhibits cell growth in human A549 lung cancer cells by blocking autophagy and inducing mitochondrial‑mediated apoptosis.
Identifieur interne : 000C43 ( Main/Exploration ); précédent : 000C42; suivant : 000C44Chloroquine inhibits cell growth in human A549 lung cancer cells by blocking autophagy and inducing mitochondrial‑mediated apoptosis.
Auteurs : Likun Liu [République populaire de Chine] ; Cuicui Han [République populaire de Chine] ; Haitao Yu [République populaire de Chine] ; Wenbin Zhu [République populaire de Chine] ; Hongxia Cui [République populaire de Chine] ; Lihong Zheng [République populaire de Chine] ; Chunjing Zhang [République populaire de Chine] ; Liling Yue [République populaire de Chine]Source :
- Oncology reports [ 1791-2431 ] ; 2018.
Descripteurs français
- KwdFr :
- Autophagie (), Cellules A549, Chloroquine (pharmacologie), Humains, Mitochondries (), Mitochondries (métabolisme), Phosphatidylinositol 3-kinases (métabolisme), Potentiel de membrane mitochondriale (), Prolifération cellulaire (), Protéines proto-oncogènes c-akt (métabolisme), Relation dose-effet des médicaments, Survie cellulaire (), Transduction du signal (), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- métabolisme : Mitochondries, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt, Tumeurs du poumon.
- pharmacologie : Chloroquine.
- traitement médicamenteux : Tumeurs du poumon.
- Autophagie, Cellules A549, Humains, Mitochondries, Potentiel de membrane mitochondriale, Prolifération cellulaire, Relation dose-effet des médicaments, Survie cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- A549 Cells, Autophagy (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Chloroquine (pharmacology), Dose-Response Relationship, Drug, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Membrane Potential, Mitochondrial (drug effects), Mitochondria (drug effects), Mitochondria (metabolism), Phosphatidylinositol 3-Kinases (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , metabolism : Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Chloroquine.
- drug effects : Autophagy, Cell Proliferation, Cell Survival, Membrane Potential, Mitochondrial, Mitochondria, Signal Transduction.
- drug therapy : Lung Neoplasms.
- metabolism : Lung Neoplasms, Mitochondria.
- A549 Cells, Dose-Response Relationship, Drug, Humans.
Abstract
Chloroquine (CQ) has been revealed to exhibit antitumor activity in several human tumors including lung cancer as mono‑ or add‑on therapy. The antitumor effect of CQ appears to depend on the tumor type, stage and genetic context. Few studies have focused on the mechanism concerning the antitumor effect of CQ monotherapy and the cause and effect relationship among autophagy, apoptosis and CQ in human lung A549 cells. Therefore, the present study aimed to identify the antitumor effect of CQ monotherapy and analyze the possible mechanism. In the present study, we demonstrated that CQ suppressed human A549 cell growth in a dose‑ and time‑dependent manner. CQ‑mediated growth inhibition in A549 cells was characterized by the targeting of the PI3K/AKT pathway, thus, inducing mitochondria‑mediated apoptosis at relatively higher concentrations by downregulating Bcl‑2 expression, increasing the expression level of Bax, decreasing mitochondrial membrane potential, releasing cytochrome c from the mitochondria into the cytosol, activating caspase‑3 and cleaving PARP. Collectively, these findings may offer a new rationale for using CQ as a lung cancer therapy drug in clinical practice.
DOI: 10.3892/or.2018.6363
PubMed: 29658606
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Han, Cuicui" sort="Han, Cuicui" uniqKey="Han C" first="Cuicui" last="Han">Cuicui Han</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Haitao" sort="Yu, Haitao" uniqKey="Yu H" first="Haitao" last="Yu">Haitao Yu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology Genetics, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biology Genetics, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Zhu, Wenbin" sort="Zhu, Wenbin" uniqKey="Zhu W" first="Wenbin" last="Zhu">Wenbin Zhu</name><affiliation wicri:level="1"><nlm:affiliation>Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Cui, Hongxia" sort="Cui, Hongxia" uniqKey="Cui H" first="Hongxia" last="Cui">Hongxia Cui</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Clinical Pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Lihong" sort="Zheng, Lihong" uniqKey="Zheng L" first="Lihong" last="Zheng">Lihong Zheng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology Genetics, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biology Genetics, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Chunjing" sort="Zhang, Chunjing" uniqKey="Zhang C" first="Chunjing" last="Zhang">Chunjing Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Biochemistry, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author><author><name sortKey="Yue, Liling" sort="Yue, Liling" uniqKey="Yue L" first="Liling" last="Yue">Liling Yue</name><affiliation wicri:level="1"><nlm:affiliation>Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar, Heilongjiang 161006</wicri:regionArea><wicri:noRegion>Heilongjiang 161006</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oncology reports</title><idno type="eISSN">1791-2431</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Autophagy (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Chloroquine (pharmacology)</term><term>Dose-Response Relationship, Drug</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (metabolism)</term><term>Membrane Potential, Mitochondrial (drug effects)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie ()</term><term>Cellules A549</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Mitochondries ()</term><term>Mitochondries (métabolisme)</term><term>Phosphatidylinositol 3-kinases (métabolisme)</term><term>Potentiel de membrane mitochondriale ()</term><term>Prolifération cellulaire ()</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire ()</term><term>Transduction du signal ()</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Membrane Potential, Mitochondrial</term><term>Mitochondria</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Mitochondries</term><term>Phosphatidylinositol 3-kinases</term><term>Protéines proto-oncogènes c-akt</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Dose-Response Relationship, Drug</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Cellules A549</term><term>Humains</term><term>Mitochondries</term><term>Potentiel de membrane mitochondriale</term><term>Prolifération cellulaire</term><term>Relation dose-effet des médicaments</term><term>Survie cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chloroquine (CQ) has been revealed to exhibit antitumor activity in several human tumors including lung cancer as mono‑ or add‑on therapy. The antitumor effect of CQ appears to depend on the tumor type, stage and genetic context. Few studies have focused on the mechanism concerning the antitumor effect of CQ monotherapy and the cause and effect relationship among autophagy, apoptosis and CQ in human lung A549 cells. Therefore, the present study aimed to identify the antitumor effect of CQ monotherapy and analyze the possible mechanism. In the present study, we demonstrated that CQ suppressed human A549 cell growth in a dose‑ and time‑dependent manner. CQ‑mediated growth inhibition in A549 cells was characterized by the targeting of the PI3K/AKT pathway, thus, inducing mitochondria‑mediated apoptosis at relatively higher concentrations by downregulating Bcl‑2 expression, increasing the expression level of Bax, decreasing mitochondrial membrane potential, releasing cytochrome c from the mitochondria into the cytosol, activating caspase‑3 and cleaving PARP. Collectively, these findings may offer a new rationale for using CQ as a lung cancer therapy drug in clinical practice.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Liu, Likun" sort="Liu, Likun" uniqKey="Liu L" first="Likun" last="Liu">Likun Liu</name></noRegion><name sortKey="Cui, Hongxia" sort="Cui, Hongxia" uniqKey="Cui H" first="Hongxia" last="Cui">Hongxia Cui</name><name sortKey="Han, Cuicui" sort="Han, Cuicui" uniqKey="Han C" first="Cuicui" last="Han">Cuicui Han</name><name sortKey="Yu, Haitao" sort="Yu, Haitao" uniqKey="Yu H" first="Haitao" last="Yu">Haitao Yu</name><name sortKey="Yue, Liling" sort="Yue, Liling" uniqKey="Yue L" first="Liling" last="Yue">Liling Yue</name><name sortKey="Zhang, Chunjing" sort="Zhang, Chunjing" uniqKey="Zhang C" first="Chunjing" last="Zhang">Chunjing Zhang</name><name sortKey="Zheng, Lihong" sort="Zheng, Lihong" uniqKey="Zheng L" first="Lihong" last="Zheng">Lihong Zheng</name><name sortKey="Zhu, Wenbin" sort="Zhu, Wenbin" uniqKey="Zhu W" first="Wenbin" last="Zhu">Wenbin Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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