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dc.contributor.authorRuiz, EJ
dc.contributor.authorLan, L
dc.contributor.authorDiefenbacher, ME
dc.contributor.authorRiising, EM
dc.contributor.authorDa Costa, C
dc.contributor.authorChakraborty, A
dc.contributor.authorHoeck, JD
dc.contributor.authorSpencer-Dene, B
dc.contributor.authorKelly, G
dc.contributor.authorDavid, J-P
dc.contributor.authorNye, E
dc.contributor.authorDownward, J
dc.contributor.authorBehrens, A
dc.date.accessioned2021-09-23T09:49:16Z
dc.date.available2021-09-23T09:49:16Z
dc.date.issued2021-07-08
dc.identifier.citationJCI insight, 2021, 6 (13)
dc.identifier.issn2379-3708
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4827
dc.identifier.eissn2379-3708
dc.identifier.doi10.1172/jci.insight.124985
dc.description.abstractThe AP-1 transcription factor c-Jun is required for Ras-driven tumorigenesis in many tissues and is considered as a classical proto-oncogene. To determine the requirement for c-Jun in a mouse model of K-RasG12D-induced lung adenocarcinoma, we inducibly deleted c-Jun in the adult lung. Surprisingly, we found that inactivation of c-Jun, or mutation of its JNK phosphorylation sites, actually increased lung tumor burden. Mechanistically, we found that protein levels of the Jun family member JunD were increased in the absence of c-Jun. In c-Jun-deficient cells, JunD phosphorylation was increased, and expression of a dominant-active JNKK2-JNK1 transgene further increased lung tumor formation. Strikingly, deletion of JunD completely abolished Ras-driven lung tumorigenesis. This work identifies JunD, not c-Jun, as the crucial substrate of JNK signaling and oncogene required for Ras-induced lung cancer.
dc.formatElectronic
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleJunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer.
dc.typeJournal Article
dcterms.dateAccepted2021-05-28
rioxxterms.versionVoR
rioxxterms.versionofrecord10.1172/jci.insight.124985
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2021-07-08
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfJCI insight
pubs.issue13
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Lung Cancer Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Lung Cancer Group
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Lung Cancer Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Lung Cancer Group
pubs.publication-statusPublished
pubs.volume6en_US
pubs.embargo.termsNot known
icr.researchteamLung Cancer Group
icr.researchteamLung Cancer Groupen_US
dc.contributor.icrauthorBehrens, Axelen
dc.contributor.icrauthorDownward, Julian David Harryen


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Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/4.0