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EFA6B regulates a stop signal for collective invasion in breast cancer

Author

Listed:
  • Racha Fayad

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Monserrat Vázquez Rojas

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Mariagrazia Partisani

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Pascal Finetti

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105)

  • Shiraz Dib

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Sophie Abelanet

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Virginie Virolle

    (CNRS UMR7277, Inserm U1091, Institut de Biologie Valrose, Université Côte D’Azur)

  • Anne Farina

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, ICEP Platform, Aix-Marseille Université UM105)

  • Olivier Cabaud

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105)

  • Marc Lopez

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105)

  • Daniel Birnbaum

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105)

  • François Bertucci

    (INSERM U1068, Centre de Recherche en Cancérologie de Marseille, Equipe Oncologie Prédictive, Aix-Marseille Université UM105)

  • Michel Franco

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

  • Frédéric Luton

    (CNRS UMR7275, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Université Côte d’Azur)

Abstract

Cancer is initiated by somatic mutations in oncogenes or tumor suppressor genes. However, additional alterations provide selective advantages to the tumor cells to resist treatment and develop metastases. Their identification is of paramount importance. Reduced expression of EFA6B (Exchange Factor for ARF6, B) is associated with breast cancer of poor prognosis. Here, we report that loss of EFA6B triggers a transcriptional reprogramming of the cell-to-ECM interaction machinery and unleashes CDC42-dependent collective invasion in collagen. In xenograft experiments, MCF10 DCIS.com cells, a DCIS-to-IDC transition model, invades faster when knocked-out for EFA6B. In addition, invasive and metastatic tumors isolated from patients have lower expression of EFA6B and display gene ontology signatures identical to those of EFA6B knock-out cells. Thus, we reveal an EFA6B-regulated molecular mechanism that controls the invasive potential of mammary cells; this finding opens up avenues for the treatment of invasive breast cancer.

Suggested Citation

  • Racha Fayad & Monserrat Vázquez Rojas & Mariagrazia Partisani & Pascal Finetti & Shiraz Dib & Sophie Abelanet & Virginie Virolle & Anne Farina & Olivier Cabaud & Marc Lopez & Daniel Birnbaum & Françoi, 2021. "EFA6B regulates a stop signal for collective invasion in breast cancer," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22522-4
    DOI: 10.1038/s41467-021-22522-4
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