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Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells

Author

Listed:
  • Nikola Arsic

    (Université de Montpellier, Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM) CNRS, UMR 5237
    Université de Montpellier)

  • Tania Slatter

    (University of Otago)

  • Gilles Gadea

    (Université de la Réunion, Unité Mixte 134 Processus Infectieux en Milieu Insulaire Tropical, INSERM Unité 1187, CNRS Unité Mixte de Recherche 9192, IRD Unité Mixte de Recherche 249. Plateforme Technologique CYROI)

  • Etienne Villain

    (Université de Montpellier, Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM) CNRS, UMR 5237
    Université de Montpellier)

  • Aurelie Fournet

    (Université de Montpellier
    Centre de Biochimie Structurale (CBS), INSERM, CNRS, 29 rue de Navacelles)

  • Marina Kazantseva

    (University of Otago)

  • Frédéric Allemand

    (Université de Montpellier
    Centre de Biochimie Structurale (CBS), INSERM, CNRS, 29 rue de Navacelles)

  • Nathalie Sibille

    (Université de Montpellier
    Centre de Biochimie Structurale (CBS), INSERM, CNRS, 29 rue de Navacelles)

  • Martial Seveno

    (Université de Montpellier
    BioCampus Montpellier, CNRS, INSERM)

  • Sylvain Rossi

    (MRI, UMS BioCampus Montpellier, CNRS, INSERM, Université de Montpellier)

  • Sunali Mehta

    (University of Otago)

  • Serge Urbach

    (Université de Montpellier
    IGF, CNRS, INSERM)

  • Jean-Christophe Bourdon

    (Dundee Cancer Centre, University of Dundee, Ninewells Hospital and Medical School)

  • Pau Bernado

    (Université de Montpellier
    Centre de Biochimie Structurale (CBS), INSERM, CNRS, 29 rue de Navacelles)

  • Andrey V. Kajava

    (Université de Montpellier, Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM) CNRS, UMR 5237
    Université de Montpellier
    Institut de Biologie Computationnelle)

  • Antony Braithwaite

    (University of Otago)

  • Pierre Roux

    (Université de Montpellier, Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM) CNRS, UMR 5237
    Université de Montpellier)

Abstract

The p53 isoform, Δ133p53β, is critical in promoting cancer. Here we report that Δ133p53β activity is regulated through an aggregation-dependent mechanism. Δ133p53β aggregates were observed in cancer cells and tumour biopsies. The Δ133p53β aggregation depends on association with interacting partners including p63 family members or the CCT chaperone complex. Depletion of the CCT complex promotes accumulation of Δ133p53β aggregates and loss of Δ133p53β dependent cancer cell invasion. In contrast, association with p63 family members recruits Δ133p53β from aggregates increasing its intracellular mobility. Our study reveals novel mechanisms of cancer progression for p53 isoforms which are regulated through sequestration in aggregates and recruitment upon association with specific partners like p63 isoforms or CCT chaperone complex, that critically influence cancer cell features like EMT, migration and invasion.

Suggested Citation

  • Nikola Arsic & Tania Slatter & Gilles Gadea & Etienne Villain & Aurelie Fournet & Marina Kazantseva & Frédéric Allemand & Nathalie Sibille & Martial Seveno & Sylvain Rossi & Sunali Mehta & Serge Urbac, 2021. "Δ133p53β isoform pro-invasive activity is regulated through an aggregation-dependent mechanism in cancer cells," Nature Communications, Nature, vol. 12(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-25550-2
    DOI: 10.1038/s41467-021-25550-2
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