Chloroquine enhances gefitinib cytotoxicity in gefitinib-resistant nonsmall cell lung cancer cells.
Identifieur interne : 000E97 ( Main/Exploration ); précédent : 000E96; suivant : 000E98Chloroquine enhances gefitinib cytotoxicity in gefitinib-resistant nonsmall cell lung cancer cells.
Auteurs : Mei-Chuan Tang [Taïwan] ; Mei-Yi Wu [Taïwan] ; Ming-Hung Hwang [Taïwan] ; Ya-Ting Chang [Taïwan] ; Hui-Ju Huang [Taïwan] ; Anya Maan-Yuh Lin [Taïwan] ; James Chih-Hsin Yang [Taïwan]Source :
- PloS one [ 1932-6203 ] ; 2015.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Antinéoplasiques (pharmacologie), Antinéoplasiques (usage thérapeutique), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (génétique), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Chloroquine (pharmacologie), Chloroquine (usage thérapeutique), Humains, Lignée cellulaire tumorale, Quinazolines (pharmacologie), Quinazolines (usage thérapeutique), Récepteurs ErbB (génétique), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (génétique), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- analogues et dérivés : Adénine.
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- génétique : Carcinome pulmonaire non à petites cellules, Récepteurs ErbB, Tumeurs du poumon.
- pharmacologie : Adénine, Antinéoplasiques, Chloroquine, Quinazolines.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- usage thérapeutique : Antinéoplasiques, Chloroquine, Quinazolines.
- Autophagie, Humains, Lignée cellulaire tumorale.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Antineoplastic Agents (pharmacology), Antineoplastic Agents (therapeutic use), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Chloroquine (pharmacology), Chloroquine (therapeutic use), ErbB Receptors (genetics), Gefitinib, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), Quinazolines (pharmacology), Quinazolines (therapeutic use).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , genetics : ErbB Receptors.
- chemical , pharmacology : Adenine, Antineoplastic Agents, Chloroquine, Quinazolines.
- chemical , therapeutic use : Antineoplastic Agents, Chloroquine, Quinazolines.
- drug effects : Autophagy.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Gefitinib, Humans.
Abstract
Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), including gefitinib, are effective for non-small cell lung cancer (NSCLC) patients with EGFR mutations. However, these patients eventually develop resistance to EGFR-TKI. The goal of the present study was to investigate the involvement of autophagy in gefitinib resistance. We developed gefitinib-resistant cells (PC-9/gef) from PC-9 cells (containing exon 19 deletion EGFR) after long-term exposure in gefitinib. PC-9/gef cells (B4 and E3) were 200-fold more resistant to gefitinib than PC-9/wt cells. Compared with PC-9/wt cells, both PC-9/gefB4 and PC-9/gefE3 cells demonstrated higher basal LC3-II levels which were inhibited by 3-methyladenine (3-MA, an autophagy inhibitor) and potentiated by chloroquine (CQ, an inhibitor of autophagolysosomes formation), indicating elevated autophagy in PC-9/gef cells. 3-MA and CQ concentration-dependently inhibited cell survival of both PC-9wt and PC-9/gef cells, suggesting that autophagy may be pro-survival. Furthermore, gefitinib increased LC3-II levels and autolysosome formation in both PC-9/wt cells and PC-9/gef cells. In PC-9/wt cells, CQ potentiated the cytotoxicity by low gefitinib (3 nM). Moreover, CQ overcame the acquired gefitinib resistance in PC-9/gef cells by enhancing gefitinib-induced cytotoxicity, activation of caspase 3 and poly (ADP-ribose) polymerase cleavage. Using an in vivo model xenografting with PC-9/wt and PC-9/gefB4 cells, oral administration of gefitinib (50 mg/kg) completely inhibited the tumor growth of PC-9/wt but not PC-9/gefB4cells. Combination of CQ (75 mg/kg, i.p.) and gefitinib was more effective than gefitinib alone in reducing the tumor growth of PC-9/gefB4. Our data suggest that inhibition of autophagy may be a therapeutic strategy to overcome acquired resistance of gefitinib in EGFR mutation NSCLC patients.
DOI: 10.1371/journal.pone.0119135
PubMed: 25807554
Affiliations:
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Department of Medical Research, Taipei-Veterans General Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan; Department of Medical Research, Taipei-Veterans General Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Yang, James Chih Hsin" sort="Yang, James Chih Hsin" uniqKey="Yang J" first="James Chih-Hsin" last="Yang">James Chih-Hsin Yang</name><affiliation wicri:level="1"><nlm:affiliation>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University and Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University and Department of Oncology, National Taiwan University Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25807554</idno><idno type="pmid">25807554</idno><idno type="doi">10.1371/journal.pone.0119135</idno><idno type="wicri:Area/PubMed/Corpus">000263</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000263</idno><idno type="wicri:Area/PubMed/Curation">000263</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000263</idno><idno type="wicri:Area/PubMed/Checkpoint">000251</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000251</idno><idno type="wicri:Area/Ncbi/Merge">000282</idno><idno type="wicri:Area/Ncbi/Curation">000282</idno><idno type="wicri:Area/Ncbi/Checkpoint">000282</idno><idno type="wicri:Area/Main/Merge">000E98</idno><idno type="wicri:Area/Main/Curation">000E97</idno><idno type="wicri:Area/Main/Exploration">000E97</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chloroquine enhances gefitinib cytotoxicity in gefitinib-resistant nonsmall cell lung cancer cells.</title><author><name sortKey="Tang, Mei Chuan" sort="Tang, Mei Chuan" uniqKey="Tang M" first="Mei-Chuan" last="Tang">Mei-Chuan Tang</name><affiliation wicri:level="1"><nlm:affiliation>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Mei Yi" sort="Wu, Mei Yi" uniqKey="Wu M" first="Mei-Yi" last="Wu">Mei-Yi Wu</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Pharmacology, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Hwang, Ming Hung" sort="Hwang, Ming Hung" uniqKey="Hwang M" first="Ming-Hung" last="Hwang">Ming-Hung Hwang</name><affiliation wicri:level="1"><nlm:affiliation>Graduate Institute of Oncology, National Taiwan University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Oncology, National Taiwan University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Chang, Ya Ting" sort="Chang, Ya Ting" uniqKey="Chang Y" first="Ya-Ting" last="Chang">Ya-Ting Chang</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Pharmacology, National Yang-Ming University, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Huang, Hui Ju" sort="Huang, Hui Ju" uniqKey="Huang H" first="Hui-Ju" last="Huang">Hui-Ju Huang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Research, Taipei-Veterans General Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Medical Research, Taipei-Veterans General Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Anya Maan Yuh" sort="Lin, Anya Maan Yuh" uniqKey="Lin A" first="Anya Maan-Yuh" last="Lin">Anya Maan-Yuh Lin</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan; Department of Medical Research, Taipei-Veterans General Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan; Department of Medical Research, Taipei-Veterans General Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Yang, James Chih Hsin" sort="Yang, James Chih Hsin" uniqKey="Yang J" first="James Chih-Hsin" last="Yang">James Chih-Hsin Yang</name><affiliation wicri:level="1"><nlm:affiliation>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University and Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>National Center of Excellence for Clinical Trial and Research, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Oncology, National Taiwan University and Department of Oncology, National Taiwan University Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Antineoplastic Agents (pharmacology)</term><term>Antineoplastic Agents (therapeutic use)</term><term>Autophagy (drug effects)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (genetics)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>Chloroquine (therapeutic use)</term><term>ErbB Receptors (genetics)</term><term>Gefitinib</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (pathology)</term><term>Quinazolines (pharmacology)</term><term>Quinazolines (therapeutic use)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénine (analogues et dérivés)</term><term>Adénine (pharmacologie)</term><term>Antinéoplasiques (pharmacologie)</term><term>Antinéoplasiques (usage thérapeutique)</term><term>Autophagie ()</term><term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term><term>Carcinome pulmonaire non à petites cellules (génétique)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Chloroquine (pharmacologie)</term><term>Chloroquine (usage thérapeutique)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Quinazolines (pharmacologie)</term><term>Quinazolines (usage thérapeutique)</term><term>Récepteurs ErbB (génétique)</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs du poumon (génétique)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>ErbB Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Quinazolines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Quinazolines</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adénine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Récepteurs ErbB</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adénine</term><term>Antinéoplasiques</term><term>Chloroquine</term><term>Quinazolines</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term><term>Chloroquine</term><term>Quinazolines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Gefitinib</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), including gefitinib, are effective for non-small cell lung cancer (NSCLC) patients with EGFR mutations. However, these patients eventually develop resistance to EGFR-TKI. The goal of the present study was to investigate the involvement of autophagy in gefitinib resistance. We developed gefitinib-resistant cells (PC-9/gef) from PC-9 cells (containing exon 19 deletion EGFR) after long-term exposure in gefitinib. PC-9/gef cells (B4 and E3) were 200-fold more resistant to gefitinib than PC-9/wt cells. Compared with PC-9/wt cells, both PC-9/gefB4 and PC-9/gefE3 cells demonstrated higher basal LC3-II levels which were inhibited by 3-methyladenine (3-MA, an autophagy inhibitor) and potentiated by chloroquine (CQ, an inhibitor of autophagolysosomes formation), indicating elevated autophagy in PC-9/gef cells. 3-MA and CQ concentration-dependently inhibited cell survival of both PC-9wt and PC-9/gef cells, suggesting that autophagy may be pro-survival. Furthermore, gefitinib increased LC3-II levels and autolysosome formation in both PC-9/wt cells and PC-9/gef cells. In PC-9/wt cells, CQ potentiated the cytotoxicity by low gefitinib (3 nM). Moreover, CQ overcame the acquired gefitinib resistance in PC-9/gef cells by enhancing gefitinib-induced cytotoxicity, activation of caspase 3 and poly (ADP-ribose) polymerase cleavage. Using an in vivo model xenografting with PC-9/wt and PC-9/gefB4 cells, oral administration of gefitinib (50 mg/kg) completely inhibited the tumor growth of PC-9/wt but not PC-9/gefB4cells. Combination of CQ (75 mg/kg, i.p.) and gefitinib was more effective than gefitinib alone in reducing the tumor growth of PC-9/gefB4. Our data suggest that inhibition of autophagy may be a therapeutic strategy to overcome acquired resistance of gefitinib in EGFR mutation NSCLC patients.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Tang, Mei Chuan" sort="Tang, Mei Chuan" uniqKey="Tang M" first="Mei-Chuan" last="Tang">Mei-Chuan Tang</name></noRegion><name sortKey="Chang, Ya Ting" sort="Chang, Ya Ting" uniqKey="Chang Y" first="Ya-Ting" last="Chang">Ya-Ting Chang</name><name sortKey="Huang, Hui Ju" sort="Huang, Hui Ju" uniqKey="Huang H" first="Hui-Ju" last="Huang">Hui-Ju Huang</name><name sortKey="Hwang, Ming Hung" sort="Hwang, Ming Hung" uniqKey="Hwang M" first="Ming-Hung" last="Hwang">Ming-Hung Hwang</name><name sortKey="Lin, Anya Maan Yuh" sort="Lin, Anya Maan Yuh" uniqKey="Lin A" first="Anya Maan-Yuh" last="Lin">Anya Maan-Yuh Lin</name><name sortKey="Wu, Mei Yi" sort="Wu, Mei Yi" uniqKey="Wu M" first="Mei-Yi" last="Wu">Mei-Yi Wu</name><name sortKey="Yang, James Chih Hsin" sort="Yang, James Chih Hsin" uniqKey="Yang J" first="James Chih-Hsin" last="Yang">James Chih-Hsin Yang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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