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Oncotarget. 2015 Jul 10;6(19):17479-90.

RhoE is required for contact inhibition and negatively regulates tumor initiation and progression.

Author information

1
Universidad CEU-Cardenal Herrera, Facultad de Ciencias de la Salud, Dep. Ciencias Biomédicas, Moncada, Spain.
2
Departament de Biologia Cellular, Fisiologia i Immunologia, Universitat Autònoma de Barcelona, Cerdanyola del Vallés, Spain.
3
Centro de Investigación Príncipe Felipe, Rho Signaling in Neuropathologies, Valencia, Spain.
4
Universidad CEU-Cardenal Herrera, Facultad de Veterinaria, Dep. PASACTA, Moncada, Spain.
5
Instituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.

Abstract

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.

KEYWORDS:

RhoE; contact inhibition; metastasis; p27Kip1; tumor suppression

PMID:
26036260
PMCID:
PMC4627322
DOI:
10.18632/oncotarget.4127
[Indexed for MEDLINE]
Free PMC Article
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