RhoE is required for contact inhibition and negatively regulates tumor initiation and progression
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Marta Hernández-Sánchez1,5,*, Enric Poch1,*, Rosa M. Guasch2, Joaquín Ortega3, Inmaculada López-Almela1, Ignacio Palmero4 and Ignacio Pérez-Roger1
1 Universidad CEU-Cardenal Herrera, Facultad de Ciencias de la Salud, Dep Ciencias Biomédicas, Moncada, Spain
2 Centro de Investigación Príncipe Felipe, Rho Signaling in Neuropathologies, Valencia, Spain
3 Universidad CEU-Cardenal Herrera, Facultad de Veterinaria, Dep. PASACTA, Moncada, Spain
4 Instituto de Investigaciones Biomédicas “Alberto Sols” CSIC-UAM, Madrid, Spain
5 Departament de Biologia cellular, Fisiologia i Immunologia, Universitat Autònoma de Barcelona, Cerdanyola del Vallés, Spain
* These authors have contributed equally to this work and should therefore be considered equal first authors
Ignacio Pérez-Roger, email:
Ignacio Palmero, email:
Keywords: contact inhibition, metastasis, RhoE, tumor suppression, p27Kip1
Received: November 01, 2014 Accepted: May 02, 2015 Published: May 12, 2015
RhoE is a small GTPase involved in the regulation of actin cytoskeleton dynamics, cell cycle and apoptosis. The role of RhoE in cancer is currently controversial, with reports of both oncogenic and tumor-suppressive functions for RhoE. Using RhoE-deficient mice, we show here that the absence of RhoE blunts contact-inhibition of growth by inhibiting p27Kip1 nuclear translocation and cooperates in oncogenic transformation of mouse primary fibroblasts. Heterozygous RhoE+/gt mice are more susceptible to chemically induced skin tumors and RhoE knock-down results in increased metastatic potential of cancer cells. These results indicate that RhoE plays a role in suppressing tumor initiation and progression.
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