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dc.date.accessioned2017-05-24T11:00:49Z
dc.date.available2017-05-24T11:00:49Z
dc.date.created2016-07-13T15:10:04Z
dc.date.issued2016
dc.identifier.citationPuvirajesinghe, Tania M. Bertucci, François Jain, Ashish Scerbo, Pierluigi Belotti, Edwige Audebert, Stéphane Sebbagh, Michael Lopez, Marc Brech, Andreas Finetti, Pascal Charafe-Jauffret, Emmanuelle Chaffanet, Max Castellano, Rémy Restouin, Audrey Marchetto, Sylvie Collette, Yves Gonçalvès, Anthony Macara, Ian Birnbaum, Daniel Kodjabachian, Laurent Johansen, Terje Borg, Jean-Paul . Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast cancer. Nature Communications. 2016, 7
dc.identifier.urihttp://hdl.handle.net/10852/55479
dc.description.abstractThe non-canonical Wnt/planar cell polarity (Wnt/PCP) pathway plays a crucial role in embryonic development. Recent work has linked defects of this pathway to breast cancer aggressiveness and proposed Wnt/PCP signalling as a therapeutic target. Here we show that the archetypal Wnt/PCP protein VANGL2 is overexpressed in basal breast cancers, associated with poor prognosis and implicated in tumour growth. We identify the scaffold p62/SQSTM1 protein as a novel VANGL2-binding partner and show its key role in an evolutionarily conserved VANGL2–p62/SQSTM1–JNK pathway. This proliferative signalling cascade is upregulated in breast cancer patients with shorter survival and can be inactivated in patient-derived xenograft cells by inhibition of the JNK pathway or by disruption of the VANGL2–p62/SQSTM1 interaction. VANGL2–JNK signalling is thus a potential target for breast cancer therapy.en_US
dc.languageEN
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleIdentification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2-JNK signalling in breast canceren_US
dc.typeJournal articleen_US
dc.creator.authorPuvirajesinghe, Tania M.
dc.creator.authorBertucci, François
dc.creator.authorJain, Ashish
dc.creator.authorScerbo, Pierluigi
dc.creator.authorBelotti, Edwige
dc.creator.authorAudebert, Stéphane
dc.creator.authorSebbagh, Michael
dc.creator.authorLopez, Marc
dc.creator.authorBrech, Andreas
dc.creator.authorFinetti, Pascal
dc.creator.authorCharafe-Jauffret, Emmanuelle
dc.creator.authorChaffanet, Max
dc.creator.authorCastellano, Rémy
dc.creator.authorRestouin, Audrey
dc.creator.authorMarchetto, Sylvie
dc.creator.authorCollette, Yves
dc.creator.authorGonçalvès, Anthony
dc.creator.authorMacara, Ian
dc.creator.authorBirnbaum, Daniel
dc.creator.authorKodjabachian, Laurent
dc.creator.authorJohansen, Terje
dc.creator.authorBorg, Jean-Paul
cristin.unitcode185,53,2,10
cristin.unitnameSenter for kreftbiomedisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2
dc.identifier.cristin1367971
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Nature Communications&rft.volume=7&rft.spage=&rft.date=2016
dc.identifier.jtitleNature Communications
dc.identifier.volume7
dc.identifier.doihttp://dx.doi.org/10.1038/ncomms10318
dc.identifier.urnURN:NBN:no-58261
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn2041-1723
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/55479/1/ncomms10318.pdf
dc.type.versionPublishedVersion


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