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Fluid shear stress activates YAP1 to promote cancer cell motility

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  • Hyun Jung Lee

    (Children’s Regenerative Medicine Program, University of Texas Health Science Center at Houston
    Center for Stem Cell and Regenerative Medicine, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston)

  • Miguel F. Diaz

    (Children’s Regenerative Medicine Program, University of Texas Health Science Center at Houston
    Center for Stem Cell and Regenerative Medicine, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston)

  • Katherine M. Price

    (Rice University)

  • Joyce A. Ozuna

    (Rice University)

  • Songlin Zhang

    (The University of Texas Medical School)

  • Eva M. Sevick-Muraca

    (Center for Molecular Imaging, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston)

  • John P. Hagan

    (University of Texas Health Science Center at Houston)

  • Pamela L. Wenzel

    (Children’s Regenerative Medicine Program, University of Texas Health Science Center at Houston
    Center for Stem Cell and Regenerative Medicine, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston)

Abstract

Mechanical stress is pervasive in egress routes of malignancy, yet the intrinsic effects of force on tumour cells remain poorly understood. Here, we demonstrate that frictional force characteristic of flow in the lymphatics stimulates YAP1 to drive cancer cell migration; whereas intensities of fluid wall shear stress (WSS) typical of venous or arterial flow inhibit taxis. YAP1, but not TAZ, is strictly required for WSS-enhanced cell movement, as blockade of YAP1, TEAD1-4 or the YAP1–TEAD interaction reduces cellular velocity to levels observed without flow. Silencing of TEAD phenocopies loss of YAP1, implicating transcriptional transactivation function in mediating force-enhanced cell migration. WSS dictates expression of a network of YAP1 effectors with executive roles in invasion, chemotaxis and adhesion downstream of the ROCK–LIMK–cofilin signalling axis. Altogether, these data implicate YAP1 as a fluid mechanosensor that functions to regulate genes that promote metastasis.

Suggested Citation

  • Hyun Jung Lee & Miguel F. Diaz & Katherine M. Price & Joyce A. Ozuna & Songlin Zhang & Eva M. Sevick-Muraca & John P. Hagan & Pamela L. Wenzel, 2017. "Fluid shear stress activates YAP1 to promote cancer cell motility," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14122
    DOI: 10.1038/ncomms14122
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    Cited by:

    1. 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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