Piezo2 channel regulates RhoA and actin cytoskeleton to promote cell mechanobiological responses
Carlos Pardo-Pastor(Universitat Pompeu Fabra), Fanny Rubio-Moscardó(Universitat Pompeu Fabra), Marina Vogel-González(Universitat Pompeu Fabra), Selma A. Serra(Universitat Pompeu Fabra), Alexandros Afthinos(Johns Hopkins University), Sanela Mrkonjić(Inserm), Olivier Destaing(Inserm), Juan F. Abenza(Institute for Bioengineering of Catalonia), José M. Fernández‐Fernández(Universitat Pompeu Fabra), Xavier Trepat(Institució Catalana de Recerca i Estudis Avançats), Corinne Albigès‐Rizo(Inserm), Κωνσταντίνος Κωνσταντόπουλος(Johns Hopkins University), Miguel A. Valverde(Universitat Pompeu Fabra)
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Abstract
influx activates RhoA to control the formation and orientation of SFs and focal adhesions (FAs). A possible mechanism for the Piezo2-mediated activation of RhoA involves the recruitment of the Fyn kinase to the cell leading edge as well as calpain activation. Knockdown of Piezo2 in BrM2 cells alters SFs, FAs, and nuclear translocation of YAP; a phenotype rescued by overexpression of dominant-positive RhoA or its downstream effector, mDia1. Consequently, hallmarks of cancer invasion and metastasis related to RhoA, actin cytoskeleton, and/or force transmission, such as migration, extracellular matrix degradation, and Serpin B2 secretion, were reduced in cells lacking Piezo2.
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