Fluid shear stress activates YAP1 to promote cancer cell motility

Hyun Jung Lee, Miguel F. Diaz, Katherine M. Price, Joyce A. Ozuna, Songlin Zhang, Eva M. Sevick-Muraca, John P. Hagan and Pamela L. Wenzel ()
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Hyun Jung Lee: Children’s Regenerative Medicine Program, University of Texas Health Science Center at Houston
Miguel F. Diaz: Children’s Regenerative Medicine Program, 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

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms14122

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