RapamycinFungusV1, Main, Exploration, bibRecord, 000F49

WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.

Identifieur interne : 000F49 ( Main/Exploration ); précédent : 000F48; suivant : 000F50

WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.

Auteurs : C-W Tsai [Taïwan] ; F J Lai ; H M Sheu ; Y S Lin ; T H Chang ; M S Jan ; S M Chen ; P C Hsu ; T T Huang ; T C Huang ; M C Sheen ; S T Chen ; W C Chang ; N S Chang ; L J Hsu

Source :

Cell death & disease [ 2041-4889 ] ; 2013.

RBID : pubmed:24008736

Descripteurs français

KwdFr :
- Apoptose (effets des médicaments et des substances chimiques), Autophagie (effets des médicaments et des substances chimiques), Carcinome épidermoïde (anatomopathologie), Carcinome épidermoïde (métabolisme), Carcinome épidermoïde (traitement médicamenteux), Carcinome épidermoïde (ultrastructure), Humains (MeSH), Lignée cellulaire tumorale (MeSH), Modèles biologiques (MeSH), Méthotrexate (pharmacologie), Méthotrexate (usage thérapeutique), Oxidoreductases (métabolisme), Oxydoréductase contenant des domaines WW (MeSH), Phagosomes (effets des médicaments et des substances chimiques), Phagosomes (métabolisme), Phagosomes (ultrastructure), Protéines suppresseurs de tumeurs (métabolisme), Protéines tumorales (métabolisme), Régulation négative (effets des médicaments et des substances chimiques), Régulation positive (effets des médicaments et des substances chimiques), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (effets des médicaments et des substances chimiques), Tumeurs de la langue (anatomopathologie), Tumeurs de la langue (métabolisme), Tumeurs de la langue (traitement médicamenteux), Tumeurs de la langue (ultrastructure).
MESH :
- anatomopathologie : Carcinome épidermoïde, Tumeurs de la langue.
- effets des médicaments et des substances chimiques : Apoptose, Autophagie, Phagosomes, Régulation négative, Régulation positive, Transduction du signal.
- métabolisme : Carcinome épidermoïde, Oxidoreductases, Phagosomes, Protéines suppresseurs de tumeurs, Protéines tumorales, Sérine-thréonine kinases TOR, Tumeurs de la langue.
- pharmacologie : Méthotrexate.
- traitement médicamenteux : Carcinome épidermoïde, Tumeurs de la langue.
- usage thérapeutique : Carcinome épidermoïde, Méthotrexate, Phagosomes, Tumeurs de la langue.
- Humains, Lignée cellulaire tumorale, Modèles biologiques, Oxydoréductase contenant des domaines WW.

English descriptors

KwdEn :
- Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Squamous Cell (drug therapy), Carcinoma, Squamous Cell (metabolism), Carcinoma, Squamous Cell (pathology), Carcinoma, Squamous Cell (ultrastructure), Cell Line, Tumor (MeSH), Down-Regulation (drug effects), Humans (MeSH), Methotrexate (pharmacology), Methotrexate (therapeutic use), Models, Biological (MeSH), Neoplasm Proteins (metabolism), Oxidoreductases (metabolism), Phagosomes (drug effects), Phagosomes (metabolism), Phagosomes (ultrastructure), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (metabolism), Tongue Neoplasms (drug therapy), Tongue Neoplasms (metabolism), Tongue Neoplasms (pathology), Tongue Neoplasms (ultrastructure), Tumor Suppressor Proteins (metabolism), Up-Regulation (drug effects), WW Domain-Containing Oxidoreductase (MeSH).
MESH :
- chemical , metabolism : Neoplasm Proteins, Oxidoreductases, TOR Serine-Threonine Kinases, Tumor Suppressor Proteins.
- chemical , pharmacology : Methotrexate.
- drug effects : Apoptosis, Autophagy, Down-Regulation, Phagosomes, Signal Transduction, Up-Regulation.
- drug therapy : Carcinoma, Squamous Cell, Tongue Neoplasms.
- metabolism : Carcinoma, Squamous Cell, Phagosomes, Tongue Neoplasms.
- pathology : Carcinoma, Squamous Cell, Tongue Neoplasms.
- chemical , therapeutic use : Methotrexate.
- ultrastructure : Carcinoma, Squamous Cell, Phagosomes, Tongue Neoplasms.
- Cell Line, Tumor, Humans, Models, Biological, WW Domain-Containing Oxidoreductase.

Abstract

Squamous cell carcinoma (SCC) cells refractory to initial chemotherapy frequently develop disease relapse and distant metastasis. We show here that tumor suppressor WW domain-containing oxidoreductase (WWOX) (also named FOR or WOX1) regulates the susceptibility of SCC to methotrexate (MTX) in vitro and cure of SCC in MTX therapy. MTX increased WWOX expression, accompanied by caspase activation and apoptosis, in MTX-sensitive SCC cell lines and tumor biopsies. Suppression by a dominant-negative or small interfering RNA targeting WWOX blocked MTX-mediated cell death in sensitive SCC-15 cells that highly expressed WWOX. In stark contrast, SCC-9 cells expressed minimum amount of WWOX protein and resisted MTX-induced apoptosis. Transiently overexpressed WWOX sensitized SCC-9 cells to apoptosis by MTX. MTX significantly downregulated autophagy-related Beclin-1, Atg12-Atg5 and LC3-II protein expression and autophagosome formation in the sensitive SCC-15, whereas autophagy remained robust in the resistant SCC-9. Mechanistically, WWOX physically interacted with mammalian target of rapamycin (mTOR), which potentiated MTX-increased phosphorylation of mTOR and its downstream substrate p70 S6 kinase, along with dramatic downregulation of the aforementioned proteins in autophagy, in SCC-15. When WWOX was knocked down in SCC-15, MTX-induced mTOR signaling and autophagy inhibition were blocked. Thus, WWOX renders SCC cells susceptible to MTX-induced apoptosis by dampening autophagy, and the failure in inducing WWOX expression leads to chemotherapeutic drug resistance.

DOI: 10.1038/cddis.2013.308
PubMed: 24008736
PubMed Central: PMC3789168

Affiliations:

Taïwan

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000F65
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Le document en format XML

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<author><name sortKey="Lin, Y S" sort="Lin, Y S" uniqKey="Lin Y" first="Y S" last="Lin">Y S Lin</name>
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<author><name sortKey="Chen, S M" sort="Chen, S M" uniqKey="Chen S" first="S M" last="Chen">S M Chen</name>
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<author><name sortKey="Huang, T T" sort="Huang, T T" uniqKey="Huang T" first="T T" last="Huang">T T Huang</name>
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<author><name sortKey="Huang, T C" sort="Huang, T C" uniqKey="Huang T" first="T C" last="Huang">T C Huang</name>
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<author><name sortKey="Sheen, M C" sort="Sheen, M C" uniqKey="Sheen M" first="M C" last="Sheen">M C Sheen</name>
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<author><name sortKey="Chen, S T" sort="Chen, S T" uniqKey="Chen S" first="S T" last="Chen">S T Chen</name>
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<idno type="eISSN">2041-4889</idno>
<imprint><date when="2013" type="published">2013</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term>
<term>Autophagy (drug effects)</term>
<term>Carcinoma, Squamous Cell (drug therapy)</term>
<term>Carcinoma, Squamous Cell (metabolism)</term>
<term>Carcinoma, Squamous Cell (pathology)</term>
<term>Carcinoma, Squamous Cell (ultrastructure)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Down-Regulation (drug effects)</term>
<term>Humans (MeSH)</term>
<term>Methotrexate (pharmacology)</term>
<term>Methotrexate (therapeutic use)</term>
<term>Models, Biological (MeSH)</term>
<term>Neoplasm Proteins (metabolism)</term>
<term>Oxidoreductases (metabolism)</term>
<term>Phagosomes (drug effects)</term>
<term>Phagosomes (metabolism)</term>
<term>Phagosomes (ultrastructure)</term>
<term>Signal Transduction (drug effects)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Tongue Neoplasms (drug therapy)</term>
<term>Tongue Neoplasms (metabolism)</term>
<term>Tongue Neoplasms (pathology)</term>
<term>Tongue Neoplasms (ultrastructure)</term>
<term>Tumor Suppressor Proteins (metabolism)</term>
<term>Up-Regulation (drug effects)</term>
<term>WW Domain-Containing Oxidoreductase (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Carcinome épidermoïde (anatomopathologie)</term>
<term>Carcinome épidermoïde (métabolisme)</term>
<term>Carcinome épidermoïde (traitement médicamenteux)</term>
<term>Carcinome épidermoïde (ultrastructure)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Modèles biologiques (MeSH)</term>
<term>Méthotrexate (pharmacologie)</term>
<term>Méthotrexate (usage thérapeutique)</term>
<term>Oxidoreductases (métabolisme)</term>
<term>Oxydoréductase contenant des domaines WW (MeSH)</term>
<term>Phagosomes (effets des médicaments et des substances chimiques)</term>
<term>Phagosomes (métabolisme)</term>
<term>Phagosomes (ultrastructure)</term>
<term>Protéines suppresseurs de tumeurs (métabolisme)</term>
<term>Protéines tumorales (métabolisme)</term>
<term>Régulation négative (effets des médicaments et des substances chimiques)</term>
<term>Régulation positive (effets des médicaments et des substances chimiques)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Tumeurs de la langue (anatomopathologie)</term>
<term>Tumeurs de la langue (métabolisme)</term>
<term>Tumeurs de la langue (traitement médicamenteux)</term>
<term>Tumeurs de la langue (ultrastructure)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neoplasm Proteins</term>
<term>Oxidoreductases</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Tumor Suppressor Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Methotrexate</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Tumeurs de la langue</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Down-Regulation</term>
<term>Phagosomes</term>
<term>Signal Transduction</term>
<term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Tongue Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term>
<term>Autophagie</term>
<term>Phagosomes</term>
<term>Régulation négative</term>
<term>Régulation positive</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Phagosomes</term>
<term>Tongue Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Oxidoreductases</term>
<term>Phagosomes</term>
<term>Protéines suppresseurs de tumeurs</term>
<term>Protéines tumorales</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs de la langue</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Tongue Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Méthotrexate</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Methotrexate</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Tumeurs de la langue</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Phagosomes</term>
<term>Tongue Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Méthotrexate</term>
<term>Phagosomes</term>
<term>Tumeurs de la langue</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Humans</term>
<term>Models, Biological</term>
<term>WW Domain-Containing Oxidoreductase</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Modèles biologiques</term>
<term>Oxydoréductase contenant des domaines WW</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Squamous cell carcinoma (SCC) cells refractory to initial chemotherapy frequently develop disease relapse and distant metastasis. We show here that tumor suppressor WW domain-containing oxidoreductase (WWOX) (also named FOR or WOX1) regulates the susceptibility of SCC to methotrexate (MTX) in vitro and cure of SCC in MTX therapy. MTX increased WWOX expression, accompanied by caspase activation and apoptosis, in MTX-sensitive SCC cell lines and tumor biopsies. Suppression by a dominant-negative or small interfering RNA targeting WWOX blocked MTX-mediated cell death in sensitive SCC-15 cells that highly expressed WWOX. In stark contrast, SCC-9 cells expressed minimum amount of WWOX protein and resisted MTX-induced apoptosis. Transiently overexpressed WWOX sensitized SCC-9 cells to apoptosis by MTX. MTX significantly downregulated autophagy-related Beclin-1, Atg12-Atg5 and LC3-II protein expression and autophagosome formation in the sensitive SCC-15, whereas autophagy remained robust in the resistant SCC-9. Mechanistically, WWOX physically interacted with mammalian target of rapamycin (mTOR), which potentiated MTX-increased phosphorylation of mTOR and its downstream substrate p70 S6 kinase, along with dramatic downregulation of the aforementioned proteins in autophagy, in SCC-15. When WWOX was knocked down in SCC-15, MTX-induced mTOR signaling and autophagy inhibition were blocked. Thus, WWOX renders SCC cells susceptible to MTX-induced apoptosis by dampening autophagy, and the failure in inducing WWOX expression leads to chemotherapeutic drug resistance.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24008736</PMID>
<DateCompleted><Year>2014</Year>
<Month>03</Month>
<Day>12</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-4889</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>4</Volume>
<PubDate><Year>2013</Year>
<Month>Sep</Month>
<Day>05</Day>
</PubDate>
</JournalIssue>
<Title>Cell death & disease</Title>
<ISOAbbreviation>Cell Death Dis</ISOAbbreviation>
</Journal>
<ArticleTitle>WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.</ArticleTitle>
<Pagination><MedlinePgn>e792</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/cddis.2013.308</ELocationID>
<Abstract><AbstractText>Squamous cell carcinoma (SCC) cells refractory to initial chemotherapy frequently develop disease relapse and distant metastasis. We show here that tumor suppressor WW domain-containing oxidoreductase (WWOX) (also named FOR or WOX1) regulates the susceptibility of SCC to methotrexate (MTX) in vitro and cure of SCC in MTX therapy. MTX increased WWOX expression, accompanied by caspase activation and apoptosis, in MTX-sensitive SCC cell lines and tumor biopsies. Suppression by a dominant-negative or small interfering RNA targeting WWOX blocked MTX-mediated cell death in sensitive SCC-15 cells that highly expressed WWOX. In stark contrast, SCC-9 cells expressed minimum amount of WWOX protein and resisted MTX-induced apoptosis. Transiently overexpressed WWOX sensitized SCC-9 cells to apoptosis by MTX. MTX significantly downregulated autophagy-related Beclin-1, Atg12-Atg5 and LC3-II protein expression and autophagosome formation in the sensitive SCC-15, whereas autophagy remained robust in the resistant SCC-9. Mechanistically, WWOX physically interacted with mammalian target of rapamycin (mTOR), which potentiated MTX-increased phosphorylation of mTOR and its downstream substrate p70 S6 kinase, along with dramatic downregulation of the aforementioned proteins in autophagy, in SCC-15. When WWOX was knocked down in SCC-15, MTX-induced mTOR signaling and autophagy inhibition were blocked. Thus, WWOX renders SCC cells susceptible to MTX-induced apoptosis by dampening autophagy, and the failure in inducing WWOX expression leads to chemotherapeutic drug resistance.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tsai</LastName>
<ForeName>C-W</ForeName>
<Initials>CW</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lai</LastName>
<ForeName>F J</ForeName>
<Initials>FJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Sheu</LastName>
<ForeName>H M</ForeName>
<Initials>HM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Y S</ForeName>
<Initials>YS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>T H</ForeName>
<Initials>TH</Initials>
</Author>
<Author ValidYN="Y"><LastName>Jan</LastName>
<ForeName>M S</ForeName>
<Initials>MS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>S M</ForeName>
<Initials>SM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Hsu</LastName>
<ForeName>P C</ForeName>
<Initials>PC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>T T</ForeName>
<Initials>TT</Initials>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>T C</ForeName>
<Initials>TC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Sheen</LastName>
<ForeName>M C</ForeName>
<Initials>MC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>S T</ForeName>
<Initials>ST</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>W C</ForeName>
<Initials>WC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>N S</ForeName>
<Initials>NS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Hsu</LastName>
<ForeName>L J</ForeName>
<Initials>LJ</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2013</Year>
<Month>09</Month>
<Day>05</Day>
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<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Cell Death Dis</MedlineTA>
<NlmUniqueID>101524092</NlmUniqueID>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D009363">Neoplasm Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D025521">Tumor Suppressor Proteins</NameOfSubstance>
</Chemical>
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   |texte=   WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.
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	Serveur d'exploration sur la rapamycine et les champignons
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WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.

WWOX suppresses autophagy for inducing apoptosis in methotrexate-treated human squamous cell carcinoma.

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