Combining AKT inhibition with chloroquine and gefitinib prevents compensatory autophagy and induces cell death in EGFR mutated NSCLC cells.
Identifieur interne : 000254 ( Ncbi/Checkpoint ); précédent : 000253; suivant : 000255Combining AKT inhibition with chloroquine and gefitinib prevents compensatory autophagy and induces cell death in EGFR mutated NSCLC cells.
Auteurs : Sivan M. Bokobza [Royaume-Uni] ; Yanyan Jiang ; Anika M. Weber ; Aoife M. Devery ; Anderson J. Ryan [Royaume-Uni]Source :
- Oncotarget [ 1949-2553 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (génétique), Carcinome pulmonaire non à petites cellules (métabolisme), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Chloroquine (administration et posologie), Chloroquine (pharmacologie), Composés hétérocycliques 3 noyaux (administration et posologie), Composés hétérocycliques 3 noyaux (pharmacologie), Femelle, Humains, Interférence par ARN, Lignée cellulaire tumorale, Mutation, Prolifération cellulaire (), Protocoles de polychimiothérapie antinéoplasique (usage thérapeutique), Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs), Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Quinazolines (administration et posologie), Quinazolines (pharmacologie), Récepteurs ErbB (antagonistes et inhibiteurs), Récepteurs ErbB (génétique), Récepteurs ErbB (métabolisme), Souris de lignée BALB C, Souris nude, Survie cellulaire (), Synergie des médicaments, Technique de Western, Tests d'activité antitumorale sur modèle de xénogreffe, Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- administration et posologie : Chloroquine, Composés hétérocycliques 3 noyaux, Quinazolines.
- antagonistes et inhibiteurs : Protéines proto-oncogènes c-akt, Récepteurs ErbB.
- génétique : Carcinome pulmonaire non à petites cellules, Protéines proto-oncogènes c-akt, Récepteurs ErbB, Tumeurs du poumon.
- métabolisme : Carcinome pulmonaire non à petites cellules, Protéines proto-oncogènes c-akt, Récepteurs ErbB, Tumeurs du poumon.
- pharmacologie : Chloroquine, Composés hétérocycliques 3 noyaux, Quinazolines.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- usage thérapeutique : Protocoles de polychimiothérapie antinéoplasique.
- Animaux, Apoptose, Autophagie, Femelle, Humains, Interférence par ARN, Lignée cellulaire tumorale, Mutation, Prolifération cellulaire, Souris de lignée BALB C, Souris nude, Survie cellulaire, Synergie des médicaments, Technique de Western, Tests d'activité antitumorale sur modèle de xénogreffe.
English descriptors
- KwdEn :
- Animals, Antineoplastic Combined Chemotherapy Protocols (therapeutic use), Apoptosis (drug effects), Autophagy (drug effects), Blotting, Western, Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Cell Survival (drug effects), Chloroquine (administration & dosage), Chloroquine (pharmacology), Drug Synergism, ErbB Receptors (antagonists & inhibitors), ErbB Receptors (genetics), ErbB Receptors (metabolism), Female, Gefitinib, Heterocyclic Compounds, 3-Ring (administration & dosage), Heterocyclic Compounds, 3-Ring (pharmacology), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Mice, Inbred BALB C, Mice, Nude, Mutation, Proto-Oncogene Proteins c-akt (antagonists & inhibitors), Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), Quinazolines (administration & dosage), Quinazolines (pharmacology), RNA Interference, Xenograft Model Antitumor Assays.
- MESH :
- chemical , administration & dosage : Chloroquine, Heterocyclic Compounds, 3-Ring, Quinazolines.
- chemical , antagonists & inhibitors : ErbB Receptors, Proto-Oncogene Proteins c-akt.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Cell Survival.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, ErbB Receptors, Lung Neoplasms, Proto-Oncogene Proteins c-akt.
- metabolism : Carcinoma, Non-Small-Cell Lung, ErbB Receptors, Lung Neoplasms, Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Chloroquine, Heterocyclic Compounds, 3-Ring, Quinazolines.
- therapeutic use : Antineoplastic Combined Chemotherapy Protocols.
- Animals, Blotting, Western, Cell Line, Tumor, Drug Synergism, Female, Gefitinib, Humans, Mice, Inbred BALB C, Mice, Nude, Mutation, RNA Interference, Xenograft Model Antitumor Assays.
Abstract
Although non-small cell lung cancer (NSCLC) patients with EGFR mutation positive (EGFR M+) tumors initially respond well to EGFR tyrosine kinase inhibitor (TKI) monotherapy, the responses are usually incomplete. In this study we show that AKT inhibition, most importantly AKT2 inhibition, synergises with EGFR TKI inhibition to increase cell killing in EGFR M+ NSCLC cells. However, our data also suggest that the synergistic pro-apoptotic effects may be stunted due to a prosurvival autophagy response induced by AKT inhibition. Consequently, inhibiting autophagy with chloroquine significantly enhanced tumor cell death induced by gefitinib and AKT inhibitors in EGFR M+ cells in vitro, and produced greater tumor shrinkage in EGFR M+ xenografts in vivo. Together, our findings suggest that adding chloroquine to EGFR and AKT inhibition has the potential to improve tumor responses in EGFR M+ NSCLC, and that selective targeting of AKT2 may provide a new treatment option in NSCLC.
DOI: 10.18632/oncotarget.2017
PubMed: 24946858
Affiliations:
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pubmed:24946858Le document en format XML
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<term>Blotting, Western</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (metabolism)</term>
<term>Cell Line, Tumor</term>
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<term>Chloroquine (administration & dosage)</term>
<term>Chloroquine (pharmacology)</term>
<term>Drug Synergism</term>
<term>ErbB Receptors (antagonists & inhibitors)</term>
<term>ErbB Receptors (genetics)</term>
<term>ErbB Receptors (metabolism)</term>
<term>Female</term>
<term>Gefitinib</term>
<term>Heterocyclic Compounds, 3-Ring (administration & dosage)</term>
<term>Heterocyclic Compounds, 3-Ring (pharmacology)</term>
<term>Humans</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Mutation</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Quinazolines (administration & dosage)</term>
<term>Quinazolines (pharmacology)</term>
<term>RNA Interference</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose ()</term>
<term>Autophagie ()</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (métabolisme)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Chloroquine (administration et posologie)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Composés hétérocycliques 3 noyaux (administration et posologie)</term>
<term>Composés hétérocycliques 3 noyaux (pharmacologie)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
<term>Prolifération cellulaire ()</term>
<term>Protocoles de polychimiothérapie antinéoplasique (usage thérapeutique)</term>
<term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Quinazolines (administration et posologie)</term>
<term>Quinazolines (pharmacologie)</term>
<term>Récepteurs ErbB (antagonistes et inhibiteurs)</term>
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<term>Récepteurs ErbB (métabolisme)</term>
<term>Souris de lignée BALB C</term>
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<term>Tumeurs du poumon (métabolisme)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
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<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Chloroquine</term>
<term>Heterocyclic Compounds, 3-Ring</term>
<term>Quinazolines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>ErbB Receptors</term>
<term>Proto-Oncogene Proteins c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Chloroquine</term>
<term>Composés hétérocycliques 3 noyaux</term>
<term>Quinazolines</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
<term>Récepteurs ErbB</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Proliferation</term>
<term>Cell Survival</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>ErbB Receptors</term>
<term>Lung Neoplasms</term>
<term>Proto-Oncogene Proteins c-akt</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Récepteurs ErbB</term>
<term>Tumeurs du poumon</term>
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<term>ErbB Receptors</term>
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<term>Récepteurs ErbB</term>
<term>Tumeurs du poumon</term>
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<term>Composés hétérocycliques 3 noyaux</term>
<term>Quinazolines</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term>
<term>Heterocyclic Compounds, 3-Ring</term>
<term>Quinazolines</term>
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<term>RNA Interference</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Apoptose</term>
<term>Autophagie</term>
<term>Femelle</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
<term>Prolifération cellulaire</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
<term>Survie cellulaire</term>
<term>Synergie des médicaments</term>
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<front><div type="abstract" xml:lang="en">Although non-small cell lung cancer (NSCLC) patients with EGFR mutation positive (EGFR M+) tumors initially respond well to EGFR tyrosine kinase inhibitor (TKI) monotherapy, the responses are usually incomplete. In this study we show that AKT inhibition, most importantly AKT2 inhibition, synergises with EGFR TKI inhibition to increase cell killing in EGFR M+ NSCLC cells. However, our data also suggest that the synergistic pro-apoptotic effects may be stunted due to a prosurvival autophagy response induced by AKT inhibition. Consequently, inhibiting autophagy with chloroquine significantly enhanced tumor cell death induced by gefitinib and AKT inhibitors in EGFR M+ cells in vitro, and produced greater tumor shrinkage in EGFR M+ xenografts in vivo. Together, our findings suggest that adding chloroquine to EGFR and AKT inhibition has the potential to improve tumor responses in EGFR M+ NSCLC, and that selective targeting of AKT2 may provide a new treatment option in NSCLC. </div>
</front>
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<affiliations><list><country><li>Royaume-Uni</li>
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<tree><noCountry><name sortKey="Devery, Aoife M" sort="Devery, Aoife M" uniqKey="Devery A" first="Aoife M" last="Devery">Aoife M. Devery</name>
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<name sortKey="Weber, Anika M" sort="Weber, Anika M" uniqKey="Weber A" first="Anika M" last="Weber">Anika M. Weber</name>
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<country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Bokobza, Sivan M" sort="Bokobza, Sivan M" uniqKey="Bokobza S" first="Sivan M" last="Bokobza">Sivan M. Bokobza</name>
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