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

被引:13
作者
Hernandez-Sanchez, Marta [1 ,5 ]
Poch, Enric [1 ]
Guasch, Rosa M. [2 ]
Ortega, Joaquin [3 ]
Lopez-Almela, Inmaculada [1 ]
Palmero, Ignacio [4 ]
Perez-Roger, Ignacio [1 ]
机构
[1] Univ CEU Cardenal Herrera, Fac Ciencias Salud, Dept Ciencias Biomed, Moncada, Spain
[2] Rho Signaling Neuropathol, Ctr Invest Principe Felipe, Valencia, Spain
[3] Univ CEU Cardenal Herrera, Fac Vet, Dept PASACTA, Moncada, Spain
[4] CSIC UAM, Inst Invest Biomed Alberto Sols, Madrid, Spain
[5] Univ Autonoma Barcelona, Dept Biol Cellular Fisiol & Immunol, Cerdanyola Del Valles, Spain
关键词
contact inhibition; metastasis; RhoE; tumor suppression; p27(Kip1); CANCER-CELL MOTILITY; ROCK-I; PROSTATE-CANCER; P27; GROWTH; PHOSPHORYLATION; IDENTIFICATION; PROLIFERATION; METASTASIS; EXPRESSION;
D O I
10.18632/oncotarget.4127
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 p27(Kip1) 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.
引用
收藏
页码:17479 / 17490
页数:12
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