Autophagy sensitivity of neuroendocrine lung tumor cells.
Identifieur interne : 001122 ( Main/Exploration ); précédent : 001121; suivant : 001123Autophagy sensitivity of neuroendocrine lung tumor cells.
Auteurs : Seung-Keun Hong [États-Unis] ; Jin-Hwan Kim ; Dmytro Starenki ; Jong-In ParkSource :
- International journal of oncology [ 1791-2423 ] ; 2013.
Descripteurs français
- KwdFr :
- Antienzymes (pharmacologie), Antipaludiques (pharmacologie), Autophagie, Carcinome pulmonaire à petites cellules (anatomopathologie), Chloroquine (pharmacologie), Composés hétérocycliques 3 noyaux (pharmacologie), Enolase (biosynthèse), Enolase (métabolisme), Humains, Interférence par ARN, Lignée cellulaire tumorale, Macrolides (pharmacologie), Naphtyridines (pharmacologie), Petit ARN interférent, Phosphorylation (), Poly(ADP-ribose) polymerases (métabolisme), Prolifération cellulaire, Protéines adaptatrices de la transduction du signal (biosynthèse), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines associées aux microtubules (biosynthèse), Protéines associées aux microtubules (métabolisme), Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs), Protéines proto-oncogènes c-akt (métabolisme), Sirolimus (pharmacologie), Survie cellulaire, Séquestosome-1, Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (génétique), Transduction du signal, Tumeurs du poumon (anatomopathologie), Tumeurs neuroendocrines (anatomopathologie).
- MESH :
- anatomopathologie : Carcinome pulmonaire à petites cellules, Tumeurs du poumon, Tumeurs neuroendocrines.
- antagonistes et inhibiteurs : Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- biosynthèse : Enolase, Protéines adaptatrices de la transduction du signal, Protéines associées aux microtubules.
- génétique : Sérine-thréonine kinases TOR.
- métabolisme : Enolase, Poly(ADP-ribose) polymerases, Protéines adaptatrices de la transduction du signal, Protéines associées aux microtubules, Protéines proto-oncogènes c-akt.
- pharmacologie : Antienzymes, Antipaludiques, Chloroquine, Composés hétérocycliques 3 noyaux, Macrolides, Naphtyridines, Sirolimus.
- Autophagie, Humains, Interférence par ARN, Lignée cellulaire tumorale, Petit ARN interférent, Phosphorylation, Prolifération cellulaire, Survie cellulaire, Séquestosome-1, Transduction du signal.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (biosynthesis), Adaptor Proteins, Signal Transducing (metabolism), Antimalarials (pharmacology), Autophagy, Cell Line, Tumor, Cell Proliferation, Cell Survival, Chloroquine (pharmacology), Enzyme Inhibitors (pharmacology), Heterocyclic Compounds, 3-Ring (pharmacology), Humans, Lung Neoplasms (pathology), Macrolides (pharmacology), Microtubule-Associated Proteins (biosynthesis), Microtubule-Associated Proteins (metabolism), Naphthyridines (pharmacology), Neuroendocrine Tumors (pathology), Phosphopyruvate Hydratase (biosynthesis), Phosphopyruvate Hydratase (metabolism), Phosphorylation (drug effects), Poly(ADP-ribose) Polymerases (metabolism), Proto-Oncogene Proteins c-akt (antagonists & inhibitors), Proto-Oncogene Proteins c-akt (metabolism), RNA Interference, RNA, Small Interfering, Sequestosome-1 Protein, Signal Transduction, Sirolimus (pharmacology), Small Cell Lung Carcinoma (pathology), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics).
- MESH :
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , biosynthesis : Adaptor Proteins, Signal Transducing, Microtubule-Associated Proteins, Phosphopyruvate Hydratase.
- chemical , genetics : TOR Serine-Threonine Kinases.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Microtubule-Associated Proteins, Phosphopyruvate Hydratase, Poly(ADP-ribose) Polymerases, Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Antimalarials, Chloroquine, Enzyme Inhibitors, Heterocyclic Compounds, 3-Ring, Macrolides, Naphthyridines, Sirolimus.
- drug effects : Phosphorylation.
- pathology : Lung Neoplasms, Neuroendocrine Tumors, Small Cell Lung Carcinoma.
- Autophagy, Cell Line, Tumor, Cell Proliferation, Cell Survival, Humans, RNA Interference, RNA, Small Interfering, Sequestosome-1 Protein, Signal Transduction.
Abstract
Neuroendocrine (NE) phenotypes characterize a spectrum of lung tumors, including low-grade typical and intermediate-grade atypical carcinoid, high-grade large-cell NE carcinoma and small cell lung carcinoma. Currently, no effective treatments are available to cure NE lung tumors, demanding identification of biological features specific to these tumors. Here, we report that autophagy has an important role for NE lung tumor cell proliferation and survival. We found that the expression levels of the autophagy marker LC3 are relatively high in a panel of lung tumor cell lines expressing high levels of neuron-specific enolase (NSE), a key NE marker in lung tumors. In response to bafilomycin A1 and chloroquine, NE lung tumor cells exhibited cytotoxicity whereas non-NE lung tumor cells exhibited cytostasis, indicating a distinct role of autophagy for NE lung tumor cell survival. Intriguingly, in certain NE lung tumor cell lines, the levels of processed LC3 (LC3-II) were inversely correlated with AKT activity. When AKT activity was inhibited using AKTi or MK2206, the levels of LC3-II and SQSTM1/p62 were increased. In contrast, torin 1, rapamycin or mTOR knockdown increased p62 levels, suggesting that these two pathways have opposing effects on autophagy in certain NE lung tumors. Moreover, inhibition of one pathway resulted in reduced activity of the other, suggesting that these two pathways crosstalk in the tumors. These results suggest that NE lung tumor cells share a common feature of autophagy and are more sensitive to autophagy inhibition than non-NE lung tumor cells.
DOI: 10.3892/ijo.2013.2136
PubMed: 24126619
Affiliations:
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uniqKey="Park J" first="Jong-In" last="Park">Jong-In Park</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24126619</idno><idno type="pmid">24126619</idno><idno type="doi">10.3892/ijo.2013.2136</idno><idno type="wicri:Area/PubMed/Corpus">000320</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000320</idno><idno type="wicri:Area/PubMed/Curation">000320</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000320</idno><idno type="wicri:Area/PubMed/Checkpoint">000334</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000334</idno><idno type="wicri:Area/Ncbi/Merge">000219</idno><idno type="wicri:Area/Ncbi/Curation">000219</idno><idno type="wicri:Area/Ncbi/Checkpoint">000219</idno><idno type="wicri:Area/Main/Merge">001123</idno><idno type="wicri:Area/Main/Curation">001122</idno><idno 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Starenki</name></author><author><name sortKey="Park, Jong In" sort="Park, Jong In" uniqKey="Park J" first="Jong-In" last="Park">Jong-In Park</name></author></analytic><series><title level="j">International journal of oncology</title><idno type="eISSN">1791-2423</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (biosynthesis)</term><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Antimalarials (pharmacology)</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Chloroquine (pharmacology)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Heterocyclic Compounds, 3-Ring (pharmacology)</term><term>Humans</term><term>Lung Neoplasms (pathology)</term><term>Macrolides (pharmacology)</term><term>Microtubule-Associated Proteins (biosynthesis)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Naphthyridines (pharmacology)</term><term>Neuroendocrine Tumors (pathology)</term><term>Phosphopyruvate Hydratase (biosynthesis)</term><term>Phosphopyruvate Hydratase (metabolism)</term><term>Phosphorylation (drug effects)</term><term>Poly(ADP-ribose) Polymerases (metabolism)</term><term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>RNA Interference</term><term>RNA, Small Interfering</term><term>Sequestosome-1 Protein</term><term>Signal Transduction</term><term>Sirolimus (pharmacology)</term><term>Small Cell Lung Carcinoma (pathology)</term><term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term><term>TOR Serine-Threonine Kinases (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antienzymes (pharmacologie)</term><term>Antipaludiques (pharmacologie)</term><term>Autophagie</term><term>Carcinome pulmonaire à petites cellules (anatomopathologie)</term><term>Chloroquine (pharmacologie)</term><term>Composés hétérocycliques 3 noyaux (pharmacologie)</term><term>Enolase (biosynthèse)</term><term>Enolase (métabolisme)</term><term>Humains</term><term>Interférence par ARN</term><term>Lignée cellulaire tumorale</term><term>Macrolides (pharmacologie)</term><term>Naphtyridines (pharmacologie)</term><term>Petit ARN interférent</term><term>Phosphorylation ()</term><term>Poly(ADP-ribose) polymerases (métabolisme)</term><term>Prolifération cellulaire</term><term>Protéines adaptatrices de la transduction du signal (biosynthèse)</term><term>Protéines adaptatrices de la transduction du signal (métabolisme)</term><term>Protéines associées aux microtubules (biosynthèse)</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Sirolimus (pharmacologie)</term><term>Survie cellulaire</term><term>Séquestosome-1</term><term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Transduction du signal</term><term>Tumeurs du poumon (anatomopathologie)</term><term>Tumeurs neuroendocrines (anatomopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Microtubule-Associated Proteins</term><term>Phosphopyruvate Hydratase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Microtubule-Associated Proteins</term><term>Phosphopyruvate Hydratase</term><term>Poly(ADP-ribose) Polymerases</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antimalarials</term><term>Chloroquine</term><term>Enzyme Inhibitors</term><term>Heterocyclic Compounds, 3-Ring</term><term>Macrolides</term><term>Naphthyridines</term><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire à petites cellules</term><term>Tumeurs du poumon</term><term>Tumeurs neuroendocrines</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Enolase</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines associées aux microtubules</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Phosphorylation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Enolase</term><term>Poly(ADP-ribose) polymerases</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines associées aux microtubules</term><term>Protéines proto-oncogènes c-akt</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term><term>Neuroendocrine Tumors</term><term>Small Cell Lung Carcinoma</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antienzymes</term><term>Antipaludiques</term><term>Chloroquine</term><term>Composés hétérocycliques 3 noyaux</term><term>Macrolides</term><term>Naphtyridines</term><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autophagy</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Humans</term><term>RNA Interference</term><term>RNA, Small Interfering</term><term>Sequestosome-1 Protein</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Humains</term><term>Interférence par ARN</term><term>Lignée cellulaire tumorale</term><term>Petit ARN interférent</term><term>Phosphorylation</term><term>Prolifération cellulaire</term><term>Survie cellulaire</term><term>Séquestosome-1</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neuroendocrine (NE) phenotypes characterize a spectrum of lung tumors, including low-grade typical and intermediate-grade atypical carcinoid, high-grade large-cell NE carcinoma and small cell lung carcinoma. Currently, no effective treatments are available to cure NE lung tumors, demanding identification of biological features specific to these tumors. Here, we report that autophagy has an important role for NE lung tumor cell proliferation and survival. We found that the expression levels of the autophagy marker LC3 are relatively high in a panel of lung tumor cell lines expressing high levels of neuron-specific enolase (NSE), a key NE marker in lung tumors. In response to bafilomycin A1 and chloroquine, NE lung tumor cells exhibited cytotoxicity whereas non-NE lung tumor cells exhibited cytostasis, indicating a distinct role of autophagy for NE lung tumor cell survival. Intriguingly, in certain NE lung tumor cell lines, the levels of processed LC3 (LC3-II) were inversely correlated with AKT activity. When AKT activity was inhibited using AKTi or MK2206, the levels of LC3-II and SQSTM1/p62 were increased. In contrast, torin 1, rapamycin or mTOR knockdown increased p62 levels, suggesting that these two pathways have opposing effects on autophagy in certain NE lung tumors. Moreover, inhibition of one pathway resulted in reduced activity of the other, suggesting that these two pathways crosstalk in the tumors. These results suggest that NE lung tumor cells share a common feature of autophagy and are more sensitive to autophagy inhibition than non-NE lung tumor cells.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Wisconsin</li></region></list><tree><noCountry><name sortKey="Kim, Jin Hwan" sort="Kim, Jin Hwan" uniqKey="Kim J" first="Jin-Hwan" last="Kim">Jin-Hwan Kim</name><name sortKey="Park, Jong In" sort="Park, Jong In" uniqKey="Park J" first="Jong-In" last="Park">Jong-In Park</name><name sortKey="Starenki, Dmytro" sort="Starenki, Dmytro" uniqKey="Starenki D" first="Dmytro" last="Starenki">Dmytro Starenki</name></noCountry><country name="États-Unis"><region name="Wisconsin"><name sortKey="Hong, Seung Keun" sort="Hong, Seung Keun" uniqKey="Hong S" first="Seung-Keun" last="Hong">Seung-Keun Hong</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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