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Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.

Identifieur interne : 000059 ( PubMed/Curation ); précédent : 000058; suivant : 000060

Protective autophagy decreases osimertinib cytotoxicity through regulation of stem cell-like properties in lung cancer.

Auteurs : Li Li [République populaire de Chine] ; Yubo Wang [République populaire de Chine] ; Lin Jiao [République populaire de Chine] ; Caiyu Lin [République populaire de Chine] ; Conghua Lu [République populaire de Chine] ; Kejun Zhang [République populaire de Chine] ; Chen Hu [République populaire de Chine] ; Junyi Ye [République populaire de Chine] ; Dadong Zhang [République populaire de Chine] ; Haiyan Wu [République populaire de Chine] ; Mingxia Feng [République populaire de Chine] ; Yong He [République populaire de Chine]

Source :

RBID : pubmed:30910592

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English descriptors

Abstract

Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.

DOI: 10.1016/j.canlet.2019.03.027
PubMed: 30910592

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<term>Acrylamides (pharmacology)</term>
<term>Aldehyde Dehydrogenase 1 (biosynthesis)</term>
<term>Aniline Compounds (pharmacology)</term>
<term>Animals</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Autophagy (drug effects)</term>
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<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>RNA Interference</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Retinal Dehydrogenase (biosynthesis)</term>
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<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Dérivés de l'aniline (pharmacologie)</term>
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<term>Humains</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
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<term>Lignée cellulaire tumorale</term>
<term>Petit ARN interférent (génétique)</term>
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<term>RNA, Small Interfering</term>
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<term>Acrylamides</term>
<term>Aniline Compounds</term>
<term>Antineoplastic Agents</term>
<term>Chloroquine</term>
<term>Protein Kinase Inhibitors</term>
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<term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
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<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr">
<term>Facteurs de transcription SOX-B1</term>
<term>Retinal dehydrogenase</term>
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<term>Autophagy</term>
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<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
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<term>Drug Resistance, Neoplasm</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Bécline-1</term>
<term>Petit ARN interférent</term>
<term>Récepteurs ErbB</term>
<term>Résistance aux médicaments antinéoplasiques</term>
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<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
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<term>Acrylamides</term>
<term>Antinéoplasiques</term>
<term>Chloroquine</term>
<term>Dérivés de l'aniline</term>
<term>Inhibiteurs de protéines kinases</term>
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<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr">
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
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<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>RNA Interference</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
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<div type="abstract" xml:lang="en">Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.</div>
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<AbstractText>Osimertinib, a third-generation epidermal growth factor receptor - tyrosine kinase inhibitor (EGFR-TKI), shows great efficacy in EGFR-mutant non-small cell lung cancer (NSCLC); however, the resistance is inevitable. Osimertinib induces autophagy in NSCLC cells, but the role of autophagy in osimertinib resistance is not clear. We discovered that enhanced autophagy is associated with osimertinib resistance in vitro and in vivo. Inhibition of autophagy enhanced osimertinib cytotoxicity in both osimertinib-resistant and sensitive cells. Moreover, osimertinib-resistant cells exhibited stem cell-like properties, whereas autophagy inhibition decreased the stemness by downregulating the expression of SOX2 and ALDH1A1. Further, we found that knockdown of Beclin-1 inhibited the stem cell-like properties and restored osimertinib cytotoxicity. Osimertinib combined with chloroquine inhibited tumor growth more effectively than alone in xenograft mice. These results reveal that autophagy plays an adverse role in osimertinib cytotoxicity through inducing stem cell-like properties. Combination therapy of EGFR-TKI and autophagy inhibitor could provide a promising strategy to improve osimertinib cytotoxicity.</AbstractText>
<CopyrightInformation>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation>
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