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Contact inhibition controls cell survival and proliferation via YAP/TAZ-autophagy axis

Author

Listed:
  • Mariana Pavel

    (Cambridge Biomedical Campus
    “Grigore T. Popa” University of Medicine and Pharmacy)

  • Maurizio Renna

    (Cambridge Biomedical Campus
    University of Naples “Federico II”)

  • So Jung Park

    (Cambridge Biomedical Campus)

  • Fiona M. Menzies

    (Cambridge Biomedical Campus)

  • Thomas Ricketts

    (Cambridge Biomedical Campus)

  • Jens Füllgrabe

    (Cambridge Biomedical Campus)

  • Avraham Ashkenazi

    (Cambridge Biomedical Campus)

  • Rebecca A. Frake

    (Cambridge Biomedical Campus)

  • Alejandro Carnicer Lombarte

    (University of Cambridge)

  • Carla F. Bento

    (Cambridge Biomedical Campus)

  • Kristian Franze

    (University of Cambridge)

  • David C. Rubinsztein

    (Cambridge Biomedical Campus
    UK Dementia Research Institute, Cambridge Biomedical Campus)

Abstract

Contact inhibition enables noncancerous cells to cease proliferation and growth when they contact each other. This characteristic is lost when cells undergo malignant transformation, leading to uncontrolled proliferation and solid tumor formation. Here we report that autophagy is compromised in contact-inhibited cells in 2D or 3D-soft extracellular matrix cultures. In such cells, YAP/TAZ fail to co-transcriptionally regulate the expression of myosin-II genes, resulting in the loss of F-actin stress fibers, which impairs autophagosome formation. The decreased proliferation resulting from contact inhibition is partly autophagy-dependent, as is their increased sensitivity to hypoxia and glucose starvation. These findings define how mechanically repressed YAP/TAZ activity impacts autophagy to contribute to core phenotypes resulting from high cell confluence that are lost in various cancers.

Suggested Citation

  • Mariana Pavel & Maurizio Renna & So Jung Park & Fiona M. Menzies & Thomas Ricketts & Jens Füllgrabe & Avraham Ashkenazi & Rebecca A. Frake & Alejandro Carnicer Lombarte & Carla F. Bento & Kristian Fra, 2018. "Contact inhibition controls cell survival and proliferation via YAP/TAZ-autophagy axis," Nature Communications, Nature, vol. 9(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05388-x
    DOI: 10.1038/s41467-018-05388-x
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    Cited by:

    1. Robin Caire & Estelle Audoux & Mireille Thomas & Elisa Dalix & Aurélien Peyron & Killian Rodriguez & Nicola Pordone & Johann Guillemot & Yann Dickerscheit & Hubert Marotte & François Vandenesch & Fréd, 2022. "YAP promotes cell-autonomous immune responses to tackle intracellular Staphylococcus aureus in vitro," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    2. Aurore Claude-Taupin & Pierre Isnard & Alessia Bagattin & Nicolas Kuperwasser & Federica Roccio & Biagina Ruscica & Nicolas Goudin & Meriem Garfa-Traoré & Alice Regnier & Lisa Turinsky & Martine Burti, 2023. "The AMPK-Sirtuin 1-YAP axis is regulated by fluid flow intensity and controls autophagy flux in kidney epithelial cells," Nature Communications, Nature, vol. 14(1), pages 1-20, December.

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