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Nature Research, Nature Communications, 1(7), 2016

DOI: 10.1038/ncomms10318

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Identification of p62/SQSTM1 as a component of non-canonical Wnt VANGL2–JNK signalling in breast cancer

Journal article published in 2016 by Tania M. Puvirajesinghe ORCID, François Bertucci ORCID, Ashish Jain, Pierluigi Scerbo, Edwige Belotti, Stéphane Audebert, Michael Sebbagh ORCID, Marc Lopez ORCID, Andreas Brech, Pascal Finetti ORCID, Emmanuelle Charafe-Jauffret ORCID, Max Chaffanet, Rémy Castellano, Audrey Restouin, Sylvie Marchetto and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Source: doi: 10.1038/ncomms10318 ; The 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.