Autophagy sensitivity of neuroendocrine lung tumor cells.
Identifieur interne : 000320 ( PubMed/Corpus ); précédent : 000319; suivant : 000321Autophagy sensitivity of neuroendocrine lung tumor cells.
Auteurs : Seung-Keun Hong ; Jin-Hwan Kim ; Dmytro Starenki ; Jong-In ParkSource :
- International journal of oncology [ 1791-2423 ] ; 2013.
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
Links to Exploration step
pubmed:24126619Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Autophagy sensitivity of neuroendocrine lung tumor cells.</title><author><name sortKey="Hong, Seung Keun" sort="Hong, Seung Keun" uniqKey="Hong S" first="Seung-Keun" last="Hong">Seung-Keun Hong</name><affiliation><nlm:affiliation>Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Kim, Jin Hwan" sort="Kim, Jin Hwan" uniqKey="Kim J" first="Jin-Hwan" last="Kim">Jin-Hwan Kim</name></author><author><name sortKey="Starenki, Dmytro" sort="Starenki, Dmytro" uniqKey="Starenki D" first="Dmytro" last="Starenki">Dmytro 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></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24126619</idno><idno 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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="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="drug effects" xml:lang="en"><term>Phosphorylation</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" 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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24126619</PMID><DateCompleted><Year>2014</Year><Month>07</Month><Day>14</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-2423</ISSN><JournalIssue CitedMedium="Internet"><Volume>43</Volume><Issue>6</Issue><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>International journal of oncology</Title><ISOAbbreviation>Int. J. Oncol.</ISOAbbreviation></Journal><ArticleTitle>Autophagy sensitivity of neuroendocrine lung tumor cells.</ArticleTitle><Pagination><MedlinePgn>2031-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3892/ijo.2013.2136</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hong</LastName><ForeName>Seung-Keun</ForeName><Initials>SK</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jin-Hwan</ForeName><Initials>JH</Initials></Author><Author ValidYN="Y"><LastName>Starenki</LastName><ForeName>Dmytro</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Jong-In</ForeName><Initials>JI</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA138441</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United 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