Vesicular stomatitis virus oncolysis is potentiated by impairing mTORC1-dependent type I IFN production.
Identifieur interne : 001372 ( Main/Exploration ); précédent : 001371; suivant : 001373Vesicular stomatitis virus oncolysis is potentiated by impairing mTORC1-dependent type I IFN production.
Auteurs : Tommy Alain [Canada] ; Xueqing Lun ; Yvan Martineau ; Polen Sean ; Bali Pulendran ; Emmanuel Petroulakis ; Franz J. Zemp ; Chantal G. Lemay ; Dominic Roy ; John C. Bell ; George Thomas ; Sara C. Kozma ; Peter A. Forsyth ; Mauro Costa-Mattioli ; Nahum SonenbergSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (MeSH), Facteurs de transcription (métabolisme), Femelle (MeSH), Gliome (génétique), Gliome (métabolisme), Gliome (thérapie), Gliome (virologie), Interféron de type I (biosynthèse), Lignée cellulaire (MeSH), Lignée cellulaire tumorale (MeSH), Protéines (MeSH), Rats (MeSH), Rats de lignée F344 (MeSH), Ribosomal Protein S6 Kinases (déficit), Ribosomal Protein S6 Kinases (métabolisme), Ribosomal Protein S6 Kinases, 90-kDa (déficit), Ribosomal Protein S6 Kinases, 90-kDa (métabolisme), Sirolimus (pharmacologie), Souris (MeSH), Souris knockout (MeSH), Stomatite vésiculeuse (génétique), Stomatite vésiculeuse (métabolisme), Stomatite vésiculeuse (virologie), Sérine-thréonine kinases TOR (MeSH), Thérapie virale de cancers (MeSH), Transplantation tumorale (MeSH), Vesiculovirus (génétique), Vesiculovirus (physiologie).
- MESH :
- biosynthèse : Interféron de type I.
- déficit : Ribosomal Protein S6 Kinases, Ribosomal Protein S6 Kinases, 90-kDa.
- génétique : Gliome, Stomatite vésiculeuse, Vesiculovirus.
- métabolisme : Facteurs de transcription, Gliome, Ribosomal Protein S6 Kinases, Ribosomal Protein S6 Kinases, 90-kDa, Stomatite vésiculeuse.
- pharmacologie : Sirolimus.
- physiologie : Vesiculovirus.
- thérapie : Gliome.
- virologie : Gliome, Stomatite vésiculeuse.
- Animaux, Complexe-1 cible mécanistique de la rapamycine, Complexes multiprotéiques, Femelle, Lignée cellulaire, Lignée cellulaire tumorale, Protéines, Rats, Rats de lignée F344, Souris, Souris knockout, Sérine-thréonine kinases TOR, Thérapie virale de cancers, Transplantation tumorale.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Line (MeSH), Cell Line, Tumor (MeSH), Female (MeSH), Glioma (genetics), Glioma (metabolism), Glioma (therapy), Glioma (virology), Interferon Type I (biosynthesis), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Multiprotein Complexes (MeSH), Neoplasm Transplantation (MeSH), Oncolytic Virotherapy (MeSH), Proteins (MeSH), Rats (MeSH), Rats, Inbred F344 (MeSH), Ribosomal Protein S6 Kinases (deficiency), Ribosomal Protein S6 Kinases (metabolism), Ribosomal Protein S6 Kinases, 90-kDa (deficiency), Ribosomal Protein S6 Kinases, 90-kDa (metabolism), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (MeSH), Transcription Factors (metabolism), Vesicular Stomatitis (genetics), Vesicular Stomatitis (metabolism), Vesicular Stomatitis (virology), Vesiculovirus (genetics), Vesiculovirus (physiology).
- MESH :
- chemical , biosynthesis : Interferon Type I.
- chemical , deficiency : Ribosomal Protein S6 Kinases, Ribosomal Protein S6 Kinases, 90-kDa.
- genetics : Glioma, Vesicular Stomatitis, Vesiculovirus.
- metabolism : Glioma, Ribosomal Protein S6 Kinases, Ribosomal Protein S6 Kinases, 90-kDa, Transcription Factors, Vesicular Stomatitis.
- chemical , pharmacology : Sirolimus.
- physiology : Vesiculovirus.
- therapy : Glioma.
- virology : Glioma, Vesicular Stomatitis.
- Animals, Cell Line, Cell Line, Tumor, Female, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Knockout, Multiprotein Complexes, Neoplasm Transplantation, Oncolytic Virotherapy, Proteins, Rats, Rats, Inbred F344, TOR Serine-Threonine Kinases.
Abstract
Oncolytic viruses constitute a promising therapy against malignant gliomas (MGs). However, virus-induced type I IFN greatly limits its clinical application. The kinase mammalian target of rapamycin (mTOR) stimulates type I IFN production via phosphorylation of its effector proteins, 4E-BPs and S6Ks. Here we show that mouse embryonic fibroblasts and mice lacking S6K1 and S6K2 are more susceptible to vesicular stomatitis virus (VSV) infection than their WT counterparts as a result of an impaired type I IFN response. We used this knowledge to employ a pharmacoviral approach to treat MGs. The highly specific inhibitor of mTOR rapamycin, in combination with an IFN-sensitive VSV-mutant strain (VSV(DeltaM51)), dramatically increased the survival of immunocompetent rats bearing MGs. More importantly, VSV(DeltaM51) selectively killed tumor, but not normal cells, in MG-bearing rats treated with rapamycin. These results demonstrate that reducing type I IFNs through inhibition of mTORC1 is an effective strategy to augment the therapeutic activity of VSV(DeltaM51).
DOI: 10.1073/pnas.0912344107
PubMed: 20080710
PubMed Central: PMC2824402
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Zemp</name></author><author><name sortKey="Lemay, Chantal G" sort="Lemay, Chantal G" uniqKey="Lemay C" first="Chantal G" last="Lemay">Chantal G. Lemay</name></author><author><name sortKey="Roy, Dominic" sort="Roy, Dominic" uniqKey="Roy D" first="Dominic" last="Roy">Dominic Roy</name></author><author><name sortKey="Bell, John C" sort="Bell, John C" uniqKey="Bell J" first="John C" last="Bell">John C. Bell</name></author><author><name sortKey="Thomas, George" sort="Thomas, George" uniqKey="Thomas G" first="George" last="Thomas">George Thomas</name></author><author><name sortKey="Kozma, Sara C" sort="Kozma, Sara C" uniqKey="Kozma S" first="Sara C" last="Kozma">Sara C. Kozma</name></author><author><name sortKey="Forsyth, Peter A" sort="Forsyth, Peter A" uniqKey="Forsyth P" first="Peter A" last="Forsyth">Peter A. Forsyth</name></author><author><name sortKey="Costa Mattioli, Mauro" sort="Costa Mattioli, Mauro" uniqKey="Costa Mattioli M" first="Mauro" last="Costa-Mattioli">Mauro Costa-Mattioli</name></author><author><name sortKey="Sonenberg, Nahum" sort="Sonenberg, Nahum" uniqKey="Sonenberg N" first="Nahum" last="Sonenberg">Nahum Sonenberg</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Line (MeSH)</term><term>Cell Line, Tumor (MeSH)</term><term>Female (MeSH)</term><term>Glioma (genetics)</term><term>Glioma (metabolism)</term><term>Glioma (therapy)</term><term>Glioma (virology)</term><term>Interferon Type I (biosynthesis)</term><term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Multiprotein Complexes (MeSH)</term><term>Neoplasm Transplantation (MeSH)</term><term>Oncolytic Virotherapy (MeSH)</term><term>Proteins (MeSH)</term><term>Rats (MeSH)</term><term>Rats, Inbred F344 (MeSH)</term><term>Ribosomal Protein S6 Kinases (deficiency)</term><term>Ribosomal Protein S6 Kinases (metabolism)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (deficiency)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (metabolism)</term><term>Sirolimus (pharmacology)</term><term>TOR Serine-Threonine Kinases (MeSH)</term><term>Transcription Factors (metabolism)</term><term>Vesicular Stomatitis (genetics)</term><term>Vesicular Stomatitis (metabolism)</term><term>Vesicular Stomatitis (virology)</term><term>Vesiculovirus (genetics)</term><term>Vesiculovirus (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term><term>Complexes multiprotéiques (MeSH)</term><term>Facteurs de transcription (métabolisme)</term><term>Femelle (MeSH)</term><term>Gliome (génétique)</term><term>Gliome (métabolisme)</term><term>Gliome (thérapie)</term><term>Gliome (virologie)</term><term>Interféron de type I (biosynthèse)</term><term>Lignée cellulaire (MeSH)</term><term>Lignée cellulaire tumorale (MeSH)</term><term>Protéines (MeSH)</term><term>Rats (MeSH)</term><term>Rats de lignée F344 (MeSH)</term><term>Ribosomal Protein S6 Kinases (déficit)</term><term>Ribosomal Protein S6 Kinases (métabolisme)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (déficit)</term><term>Ribosomal Protein S6 Kinases, 90-kDa (métabolisme)</term><term>Sirolimus (pharmacologie)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Stomatite vésiculeuse (génétique)</term><term>Stomatite vésiculeuse (métabolisme)</term><term>Stomatite vésiculeuse (virologie)</term><term>Sérine-thréonine kinases TOR (MeSH)</term><term>Thérapie virale de cancers (MeSH)</term><term>Transplantation tumorale (MeSH)</term><term>Vesiculovirus (génétique)</term><term>Vesiculovirus (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Ribosomal Protein S6 Kinases</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron de type I</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Ribosomal Protein S6 Kinases</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Glioma</term><term>Vesicular Stomatitis</term><term>Vesiculovirus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Gliome</term><term>Stomatite vésiculeuse</term><term>Vesiculovirus</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Glioma</term><term>Ribosomal Protein S6 Kinases</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term><term>Transcription Factors</term><term>Vesicular Stomatitis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Gliome</term><term>Ribosomal Protein S6 Kinases</term><term>Ribosomal Protein S6 Kinases, 90-kDa</term><term>Stomatite vésiculeuse</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Vesiculovirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Vesiculovirus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Glioma</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Gliome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Gliome</term><term>Stomatite vésiculeuse</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Glioma</term><term>Vesicular Stomatitis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cell Line, Tumor</term><term>Female</term><term>Mechanistic Target of Rapamycin Complex 1</term><term>Mice</term><term>Mice, Knockout</term><term>Multiprotein Complexes</term><term>Neoplasm Transplantation</term><term>Oncolytic Virotherapy</term><term>Proteins</term><term>Rats</term><term>Rats, Inbred F344</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Complexes multiprotéiques</term><term>Femelle</term><term>Lignée cellulaire</term><term>Lignée cellulaire tumorale</term><term>Protéines</term><term>Rats</term><term>Rats de lignée F344</term><term>Souris</term><term>Souris knockout</term><term>Sérine-thréonine kinases TOR</term><term>Thérapie virale de cancers</term><term>Transplantation tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oncolytic viruses constitute a promising therapy against malignant gliomas (MGs). However, virus-induced type I IFN greatly limits its clinical application. The kinase mammalian target of rapamycin (mTOR) stimulates type I IFN production via phosphorylation of its effector proteins, 4E-BPs and S6Ks. Here we show that mouse embryonic fibroblasts and mice lacking S6K1 and S6K2 are more susceptible to vesicular stomatitis virus (VSV) infection than their WT counterparts as a result of an impaired type I IFN response. We used this knowledge to employ a pharmacoviral approach to treat MGs. The highly specific inhibitor of mTOR rapamycin, in combination with an IFN-sensitive VSV-mutant strain (VSV(DeltaM51)), dramatically increased the survival of immunocompetent rats bearing MGs. More importantly, VSV(DeltaM51) selectively killed tumor, but not normal cells, in MG-bearing rats treated with rapamycin. These results demonstrate that reducing type I IFNs through inhibition of mTORC1 is an effective strategy to augment the therapeutic activity of VSV(DeltaM51).</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20080710</PMID><DateCompleted><Year>2010</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>107</Volume><Issue>4</Issue><PubDate><Year>2010</Year><Month>Jan</Month><Day>26</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation></Journal><ArticleTitle>Vesicular stomatitis virus oncolysis is potentiated by impairing mTORC1-dependent type I IFN production.</ArticleTitle><Pagination><MedlinePgn>1576-81</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.0912344107</ELocationID><Abstract><AbstractText>Oncolytic viruses constitute a promising therapy against malignant gliomas (MGs). However, virus-induced type I IFN greatly limits its clinical application. The kinase mammalian target of rapamycin (mTOR) stimulates type I IFN production via phosphorylation of its effector proteins, 4E-BPs and S6Ks. Here we show that mouse embryonic fibroblasts and mice lacking S6K1 and S6K2 are more susceptible to vesicular stomatitis virus (VSV) infection than their WT counterparts as a result of an impaired type I IFN response. We used this knowledge to employ a pharmacoviral approach to treat MGs. The highly specific inhibitor of mTOR rapamycin, in combination with an IFN-sensitive VSV-mutant strain (VSV(DeltaM51)), dramatically increased the survival of immunocompetent rats bearing MGs. More importantly, VSV(DeltaM51) selectively killed tumor, but not normal cells, in MG-bearing rats treated with rapamycin. These results demonstrate that reducing type I IFNs through inhibition of mTORC1 is an effective strategy to augment the therapeutic activity of VSV(DeltaM51).</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alain</LastName><ForeName>Tommy</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Goodman Cancer Center, McGill University, Montreal, QC H3G 1Y6, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lun</LastName><ForeName>XueQing</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Martineau</LastName><ForeName>Yvan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Sean</LastName><ForeName>Polen</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Pulendran</LastName><ForeName>Bali</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Petroulakis</LastName><ForeName>Emmanuel</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Zemp</LastName><ForeName>Franz J</ForeName><Initials>FJ</Initials></Author><Author ValidYN="Y"><LastName>Lemay</LastName><ForeName>Chantal G</ForeName><Initials>CG</Initials></Author><Author ValidYN="Y"><LastName>Roy</LastName><ForeName>Dominic</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Bell</LastName><ForeName>John C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Thomas</LastName><ForeName>George</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Kozma</LastName><ForeName>Sara C</ForeName><Initials>SC</Initials></Author><Author ValidYN="Y"><LastName>Forsyth</LastName><ForeName>Peter A</ForeName><Initials>PA</Initials></Author><Author ValidYN="Y"><LastName>Costa-Mattioli</LastName><ForeName>Mauro</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Sonenberg</LastName><ForeName>Nahum</ForeName><Initials>N</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>01</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007370">Interferon Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046912">Multiprotein 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Zemp</name></noCountry><country name="Canada"><region name="Québec"><name sortKey="Alain, Tommy" sort="Alain, Tommy" uniqKey="Alain T" first="Tommy" last="Alain">Tommy Alain</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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