ChloroquineV1, Ncbi, Merge, bibRecord, 000348

MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors.

Identifieur interne : 000348 ( Ncbi/Merge ); précédent : 000347; suivant : 000349

MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors.

Auteurs : Sacha I. Rothschild [Suisse] ; Oliver Gautschi [Suisse] ; Jasmin Batliner [Suisse] ; Mathias Gugger [Suisse] ; Martin F. Fey [Suisse] ; Mario P. Tschan [Suisse]

Source :

Lung cancer (Amsterdam, Netherlands) [ 1872-8332 ] ; 2017.

RBID : pubmed:27372519

Descripteurs français

English descriptors

KwdEn :
- Adenocarcinoma (drug therapy), Adenocarcinoma (genetics), Adenocarcinoma (pathology), Adenocarcinoma of Lung, Autophagy (drug effects), Autophagy-Related Protein-1 Homolog (genetics), Benzodioxoles (pharmacology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (pathology), Cell Movement (drug effects), Cell Survival (drug effects), Dasatinib (pharmacology), Down-Regulation (drug effects), Humans, Intracellular Signaling Peptides and Proteins (genetics), Lung (pathology), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), MicroRNAs (genetics), Microtubule-Associated Proteins, Protein Kinase Inhibitors (pharmacology), Quinazolines (pharmacology), RNA, Small Interfering, Signal Transduction (drug effects), src-Family Kinases (antagonists & inhibitors), src-Family Kinases (metabolism), src-Family Kinases (pharmacology).
MESH :
- chemical , antagonists & inhibitors : src-Family Kinases.
- chemical , genetics : Autophagy-Related Protein-1 Homolog, Intracellular Signaling Peptides and Proteins, MicroRNAs.
- drug effects : Autophagy, Cell Movement, Cell Survival, Down-Regulation, Signal Transduction.
- drug therapy : Adenocarcinoma, Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Adenocarcinoma, Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- chemical , metabolism : src-Family Kinases.
- pathology : Adenocarcinoma, Carcinoma, Non-Small-Cell Lung, Lung, Lung Neoplasms.
- chemical , pharmacology : Benzodioxoles, Dasatinib, Protein Kinase Inhibitors, Quinazolines, src-Family Kinases.
- Adenocarcinoma of Lung, Humans, Microtubule-Associated Proteins, RNA, Small Interfering.

Abstract

Src tyrosine kinase inhibitors (TKIs) significantly inhibit cell migration and invasion in lung cancer cell lines with minor cytotoxic effects. In clinical trials, however, they show modest activity in combination with chemotherapeutic agents. Possible resistance mechanisms include the induction of cytoprotective autophagy upon Src inhibition. Autophagy is a cellular recycling process that allows cell survival in response to a variety of stress stimuli including responses to various treatments.

DOI: 10.1016/j.lungcan.2016.06.004
PubMed: 27372519

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pubmed:27372519

Le document en format XML

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<author><name sortKey="Rothschild, Sacha I" sort="Rothschild, Sacha I" uniqKey="Rothschild S" first="Sacha I" last="Rothschild">Sacha I. Rothschild</name>
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<term>Adenocarcinoma (genetics)</term>
<term>Adenocarcinoma (pathology)</term>
<term>Adenocarcinoma of Lung</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy-Related Protein-1 Homolog (genetics)</term>
<term>Benzodioxoles (pharmacology)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Movement (drug effects)</term>
<term>Cell Survival (drug effects)</term>
<term>Dasatinib (pharmacology)</term>
<term>Down-Regulation (drug effects)</term>
<term>Humans</term>
<term>Intracellular Signaling Peptides and Proteins (genetics)</term>
<term>Lung (pathology)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (pathology)</term>
<term>MicroRNAs (genetics)</term>
<term>Microtubule-Associated Proteins</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>Quinazolines (pharmacology)</term>
<term>RNA, Small Interfering</term>
<term>Signal Transduction (drug effects)</term>
<term>src-Family Kinases (antagonists & inhibitors)</term>
<term>src-Family Kinases (metabolism)</term>
<term>src-Family Kinases (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adénocarcinome (anatomopathologie)</term>
<term>Adénocarcinome (génétique)</term>
<term>Adénocarcinome (traitement médicamenteux)</term>
<term>Autophagie ()</term>
<term>Benzodioxoles (pharmacologie)</term>
<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Dasatinib (pharmacologie)</term>
<term>Homologue de la protéine-1 associée à l'autophagie (génétique)</term>
<term>Humains</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
<term>Mouvement cellulaire ()</term>
<term>Petit ARN interférent</term>
<term>Poumon (anatomopathologie)</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines et peptides de signalisation intracellulaire (génétique)</term>
<term>Quinazolines (pharmacologie)</term>
<term>Régulation négative ()</term>
<term>Survie cellulaire ()</term>
<term>Transduction du signal ()</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
<term>microARN (génétique)</term>
<term>src-Family kinases (antagonistes et inhibiteurs)</term>
<term>src-Family kinases (métabolisme)</term>
<term>src-Family kinases (pharmacologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>src-Family Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein-1 Homolog</term>
<term>Intracellular Signaling Peptides and Proteins</term>
<term>MicroRNAs</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Adénocarcinome</term>
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Poumon</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>src-Family kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Cell Movement</term>
<term>Cell Survival</term>
<term>Down-Regulation</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma</term>
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma</term>
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adénocarcinome</term>
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Homologue de la protéine-1 associée à l'autophagie</term>
<term>Protéines et peptides de signalisation intracellulaire</term>
<term>Tumeurs du poumon</term>
<term>microARN</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>src-Family Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>src-Family kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term>
<term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Benzodioxoles</term>
<term>Dasatinib</term>
<term>Inhibiteurs de protéines kinases</term>
<term>Quinazolines</term>
<term>src-Family kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzodioxoles</term>
<term>Dasatinib</term>
<term>Protein Kinase Inhibitors</term>
<term>Quinazolines</term>
<term>src-Family Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Adénocarcinome</term>
<term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adenocarcinoma of Lung</term>
<term>Humans</term>
<term>Microtubule-Associated Proteins</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term>
<term>Humains</term>
<term>Mouvement cellulaire</term>
<term>Petit ARN interférent</term>
<term>Protéines associées aux microtubules</term>
<term>Régulation négative</term>
<term>Survie cellulaire</term>
<term>Transduction du signal</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Src tyrosine kinase inhibitors (TKIs) significantly inhibit cell migration and invasion in lung cancer cell lines with minor cytotoxic effects. In clinical trials, however, they show modest activity in combination with chemotherapeutic agents. Possible resistance mechanisms include the induction of cytoprotective autophagy upon Src inhibition. Autophagy is a cellular recycling process that allows cell survival in response to a variety of stress stimuli including responses to various treatments.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27372519</PMID>
<DateCompleted><Year>2017</Year>
<Month>11</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>02</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8332</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>107</Volume>
<PubDate><Year>2017</Year>
<Month>05</Month>
</PubDate>
</JournalIssue>
<Title>Lung cancer (Amsterdam, Netherlands)</Title>
<ISOAbbreviation>Lung Cancer</ISOAbbreviation>
</Journal>
<ArticleTitle>MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors.</ArticleTitle>
<Pagination><MedlinePgn>73-83</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0169-5002(16)30362-2</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lungcan.2016.06.004</ELocationID>
<Abstract><AbstractText Label="OBJECTIVES">Src tyrosine kinase inhibitors (TKIs) significantly inhibit cell migration and invasion in lung cancer cell lines with minor cytotoxic effects. In clinical trials, however, they show modest activity in combination with chemotherapeutic agents. Possible resistance mechanisms include the induction of cytoprotective autophagy upon Src inhibition. Autophagy is a cellular recycling process that allows cell survival in response to a variety of stress stimuli including responses to various treatments.</AbstractText>
<AbstractText Label="MATERIAL AND METHODS">We screened autophagic activity in A549, H460, and H1299 NSCLC cell lines treated with two different Src-TKIs (saracatinib, dasatinib) or shRNA targeting SRC. The autophagy response was determined by LC3B-I to -II conversion, increased ULK1 epxression and increased GFP-LC3B dot formation. Autophagy was inhibited by pharmacological (bafilomycin A, chloroquine) or genetic (ULK1 shRNA) means. Expression of miR-106a and miR-20b was analyzed by qPCR, and we used different lentivral vectors for ectopic expression of either miR-106a mimetics, anti-sense miR-106a or different miR-106a-363 cluster constructs.</AbstractText>
<AbstractText Label="RESULTS">In the current study we found that Src-TKIs induce autophagy in lung adenocarcinoma cell lines and that a combination of autophagy and Src tyrosine kinase inhibition results in cell death. Moreover, Src-TKI induced autophagy depends on the induction of the key autophagy kinase ULK1. This ULK1 upregulation is caused by downregulation of the ULK1-targeting microRNA-106a. An inverse correlation of miR-106a and ULK1 expression was seen in lung adenocarcinoma. Accordingly, ectopic expression of miR-106a in combination with Src-TKI treatment resulted in significant cell death as compared to control transduced cells.</AbstractText>
<AbstractText Label="CONCLUSIONS">Autophagy protects lung adenocarcinoma cells from Src-TKIs via a newly identified miR-106a-ULK1 signaling pathway. The combined inhibition of Src and ULK1/autophagy might represent a promising treatment option for future clinical trials. Lastly, our data might challenge the term "oncogenic" miR-106a as it can promote sensitivity to Src-TKIs thereby underlining the context-dependent function of miRNAs.</AbstractText>
<CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rothschild</LastName>
<ForeName>Sacha I</ForeName>
<Initials>SI</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Inselspital, Bern University Hospital, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland; Department Internal Medicine, Medical Oncology, University Hospital Basel, Basel, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gautschi</LastName>
<ForeName>Oliver</ForeName>
<Initials>O</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Inselspital, Bern University Hospital, Switzerland; Medical Oncology, Cantonal Hospital, Luzern, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Batliner</LastName>
<ForeName>Jasmin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Clinical Research, University of Bern, Bern, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gugger</LastName>
<ForeName>Mathias</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fey</LastName>
<ForeName>Martin F</ForeName>
<Initials>MF</Initials>
<AffiliationInfo><Affiliation>Department of Medical Oncology, Inselspital, Bern University Hospital, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tschan</LastName>
<ForeName>Mario P</ForeName>
<Initials>MP</Initials>
<AffiliationInfo><Affiliation>Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland. Electronic address: mario.tschan@pathology.unibe.ch.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>06</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Ireland</Country>
<MedlineTA>Lung Cancer</MedlineTA>
<NlmUniqueID>8800805</NlmUniqueID>
<ISSNLinking>0169-5002</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D052117">Benzodioxoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047908">Intracellular Signaling Peptides and Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C502070">MAP1LC3B protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C542541">MIRN106 microRNA, human</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000230" MajorTopicYN="N">Adenocarcinoma</DescriptorName>
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</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Autophagy</Keyword>
<Keyword MajorTopicYN="Y">NSCLC</Keyword>
<Keyword MajorTopicYN="Y">Src tyrosine kinase inhibitor</Keyword>
<Keyword MajorTopicYN="Y">ULK1</Keyword>
<Keyword MajorTopicYN="Y">miR-106a</Keyword>
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<Month>05</Month>
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<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
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<region><li>Canton de Berne</li>
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<orgName><li>Université de Berne</li>
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<tree><country name="Suisse"><noRegion><name sortKey="Rothschild, Sacha I" sort="Rothschild, Sacha I" uniqKey="Rothschild S" first="Sacha I" last="Rothschild">Sacha I. Rothschild</name>
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MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors.

MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors.

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