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

First Author  Hernández-Sánchez M Year  2015
Journal  Oncotarget Volume  6
Issue  19 Pages  17479-90
PubMed ID  26036260 Mgi Jnum  J:251215
Mgi Id  MGI:6103147 Doi  10.18632/oncotarget.4127
Citation  Hernandez-Sanchez M, et al. (2015) RhoE is required for contact inhibition and negatively regulates tumor initiation and progression. Oncotarget 6(19):17479-90
abstractText  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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