Blocking autophagy improves the anti-tumor activity of afatinib in lung adenocarcinoma with activating EGFR mutations in vitro and in vivo.
Identifieur interne : 000D26 ( Main/Exploration ); précédent : 000D25; suivant : 000D27Blocking autophagy improves the anti-tumor activity of afatinib in lung adenocarcinoma with activating EGFR mutations in vitro and in vivo.
Auteurs : Xiangxiang Hu [République populaire de Chine] ; Si Shi [République populaire de Chine] ; Huan Wang [République populaire de Chine] ; Xiaochen Yu [République populaire de Chine] ; Qian Wang [République populaire de Chine] ; Shanshan Jiang [République populaire de Chine] ; Dianwen Ju [République populaire de Chine] ; Li Ye [République populaire de Chine] ; Meiqing Feng [République populaire de Chine]Source :
- Scientific reports [ 2045-2322 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (), Apoptose (génétique), Autophagie (), Autophagie (génétique), Caspase-3 (métabolisme), Espèces réactives de l'oxygène (métabolisme), Humains, Inhibiteurs de protéines kinases (pharmacologie), Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Protéines proto-oncogènes c-akt (métabolisme), Récepteurs ErbB (antagonistes et inhibiteurs), Récepteurs ErbB (génétique), Souris, Sérine-thréonine kinases TOR (métabolisme), Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal ().
- MESH :
- antagonistes et inhibiteurs : Récepteurs ErbB.
- génétique : Apoptose, Autophagie, Récepteurs ErbB.
- métabolisme : Caspase-3, Espèces réactives de l'oxygène, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Inhibiteurs de protéines kinases.
- Animaux, Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Souris, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.
English descriptors
- KwdEn :
- Adenocarcinoma of Lung (genetics), Adenocarcinoma of Lung (metabolism), Adenocarcinoma of Lung (pathology), Afatinib (pharmacology), Animals, Apoptosis (drug effects), Apoptosis (genetics), Autophagy (drug effects), Autophagy (genetics), Caspase 3 (metabolism), Cell Line, Tumor, Disease Models, Animal, ErbB Receptors (antagonists & inhibitors), ErbB Receptors (genetics), Humans, Mice, Protein Kinase Inhibitors (pharmacology), Proto-Oncogene Proteins c-akt (metabolism), Reactive Oxygen Species (metabolism), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (metabolism), Xenograft Model Antitumor Assays.
- MESH :
- chemical , antagonists & inhibitors : ErbB Receptors.
- chemical , genetics : ErbB Receptors.
- chemical , metabolism : Caspase 3, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Afatinib, Protein Kinase Inhibitors.
- drug effects : Apoptosis, Autophagy, Signal Transduction.
- genetics : Adenocarcinoma of Lung, Apoptosis, Autophagy.
- metabolism : Adenocarcinoma of Lung.
- pathology : Adenocarcinoma of Lung.
- Animals, Cell Line, Tumor, Disease Models, Animal, Humans, Mice, Xenograft Model Antitumor Assays.
Abstract
Afatinib, a second-generation tyrosine kinase inhibitor (TKI), has been approved for the treatment of advanced EGFR-mutant non-small cell lung cancer (NSCLC). However, afatinib's clinical application is still hampered by acquired resistance. Recently, autophagy is considered as an important mechanism of resistance to TKI. Herein, we investigated the autophagy induction as well as its influence on anti-lung adenocarcinoma activity of afatinib in two activating EGFR-mutants H1975 and H1650 cells. First, Growth inhibition and caspase-dependent apoptosis were observed in afatinib-treated H1975 and H1650 cells. Then we confirmed afatinib-induced autophagy in H1975 and H1650 cells. Importantly, autophagy inhibition using chloroquine (CQ) and 3-MA enhanced the cytotoxicity of afatinib, elucidating the cytoprotective role of autophagy in lung adenocarcinoma therapy with afatinib. Further study suggested that Akt/mTOR and Erk signaling pathways were involved in afatinib-induced autophagy, and reactive oxygen species (ROS) acted as an intracellular transducer regulating both autophagy and apoptosis in afatinib-treated H1975 and H1650 cells. Moreover, the in vivo experiment in xenograft model using H1975 cell line confirmed the enhanced anti-lung adenocarcinoma efficacy of afatinib when combined with autophagy inhibitor CQ. Thus, blocking autophagy may be a promising strategy to overcome resistance and increase sensitivity to afatinib in lung adenocarcinoma harboring activating EGFR mutations.
DOI: 10.1038/s41598-017-04258-8
PubMed: 28676644
Affiliations:
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Le document en format XML
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Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Shi, Si" sort="Shi, Si" uniqKey="Shi S" first="Si" last="Shi">Si Shi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Huan" sort="Wang, Huan" uniqKey="Wang H" first="Huan" last="Wang">Huan Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Xiaochen" sort="Yu, Xiaochen" uniqKey="Yu X" first="Xiaochen" last="Yu">Xiaochen Yu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Qian" sort="Wang, Qian" uniqKey="Wang Q" first="Qian" last="Wang">Qian Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Jiang, Shanshan" sort="Jiang, Shanshan" uniqKey="Jiang S" first="Shanshan" last="Jiang">Shanshan Jiang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Ye, Li" sort="Ye, Li" uniqKey="Ye L" first="Li" last="Ye">Li Ye</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China. yelil@fudan.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author><author><name sortKey="Feng, Meiqing" sort="Feng, Meiqing" uniqKey="Feng M" first="Meiqing" last="Feng">Meiqing Feng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203, China. fmq@fudan.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiological & Biochemical Pharmacy, School of Pharmacy, Fudan University, Shanghai, 201203</wicri:regionArea><wicri:noRegion>201203</wicri:noRegion></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma of Lung (genetics)</term><term>Adenocarcinoma of Lung (metabolism)</term><term>Adenocarcinoma of Lung (pathology)</term><term>Afatinib (pharmacology)</term><term>Animals</term><term>Apoptosis (drug effects)</term><term>Apoptosis (genetics)</term><term>Autophagy (drug effects)</term><term>Autophagy (genetics)</term><term>Caspase 3 (metabolism)</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>ErbB Receptors (antagonists & inhibitors)</term><term>ErbB Receptors (genetics)</term><term>Humans</term><term>Mice</term><term>Protein Kinase Inhibitors (pharmacology)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (drug effects)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Apoptose ()</term><term>Apoptose (génétique)</term><term>Autophagie ()</term><term>Autophagie (génétique)</term><term>Caspase-3 (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Inhibiteurs de protéines kinases (pharmacologie)</term><term>Lignée cellulaire tumorale</term><term>Modèles animaux de maladie humaine</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Récepteurs ErbB (antagonistes et inhibiteurs)</term><term>Récepteurs ErbB (génétique)</term><term>Souris</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term><term>Transduction du signal ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>ErbB Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>ErbB Receptors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term><term>Proto-Oncogene Proteins c-akt</term><term>Reactive Oxygen Species</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Afatinib</term><term>Protein Kinase Inhibitors</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteurs ErbB</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma of Lung</term><term>Apoptosis</term><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Récepteurs ErbB</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma of Lung</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Espèces réactives de l'oxygène</term><term>Protéines proto-oncogènes c-akt</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma of Lung</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Inhibiteurs de protéines kinases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Afatinib, a second-generation tyrosine kinase inhibitor (TKI), has been approved for the treatment of advanced EGFR-mutant non-small cell lung cancer (NSCLC). However, afatinib's clinical application is still hampered by acquired resistance. Recently, autophagy is considered as an important mechanism of resistance to TKI. Herein, we investigated the autophagy induction as well as its influence on anti-lung adenocarcinoma activity of afatinib in two activating EGFR-mutants H1975 and H1650 cells. First, Growth inhibition and caspase-dependent apoptosis were observed in afatinib-treated H1975 and H1650 cells. Then we confirmed afatinib-induced autophagy in H1975 and H1650 cells. Importantly, autophagy inhibition using chloroquine (CQ) and 3-MA enhanced the cytotoxicity of afatinib, elucidating the cytoprotective role of autophagy in lung adenocarcinoma therapy with afatinib. Further study suggested that Akt/mTOR and Erk signaling pathways were involved in afatinib-induced autophagy, and reactive oxygen species (ROS) acted as an intracellular transducer regulating both autophagy and apoptosis in afatinib-treated H1975 and H1650 cells. Moreover, the in vivo experiment in xenograft model using H1975 cell line confirmed the enhanced anti-lung adenocarcinoma efficacy of afatinib when combined with autophagy inhibitor CQ. Thus, blocking autophagy may be a promising strategy to overcome resistance and increase sensitivity to afatinib in lung adenocarcinoma harboring activating EGFR mutations.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Hu, Xiangxiang" sort="Hu, Xiangxiang" uniqKey="Hu X" first="Xiangxiang" last="Hu">Xiangxiang Hu</name></noRegion><name sortKey="Feng, Meiqing" sort="Feng, Meiqing" uniqKey="Feng M" first="Meiqing" last="Feng">Meiqing Feng</name><name sortKey="Jiang, Shanshan" sort="Jiang, Shanshan" uniqKey="Jiang S" first="Shanshan" last="Jiang">Shanshan Jiang</name><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><name sortKey="Shi, Si" sort="Shi, Si" uniqKey="Shi S" first="Si" last="Shi">Si Shi</name><name sortKey="Wang, Huan" sort="Wang, Huan" uniqKey="Wang H" first="Huan" last="Wang">Huan Wang</name><name sortKey="Wang, Qian" sort="Wang, Qian" uniqKey="Wang Q" first="Qian" last="Wang">Qian Wang</name><name sortKey="Ye, Li" sort="Ye, Li" uniqKey="Ye L" first="Li" last="Ye">Li Ye</name><name sortKey="Yu, Xiaochen" sort="Yu, Xiaochen" uniqKey="Yu X" first="Xiaochen" last="Yu">Xiaochen Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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