Failsafe program escape and EMT: A deleterious partnership

被引:26
作者
Ansieau, Stephane [1 ,2 ,3 ,4 ]
Courtois-Cox, Stephanie [1 ,2 ,3 ,4 ]
Morel, Anne-Pierre [1 ,2 ,3 ,4 ,5 ]
Puisieux, Alain [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] Ctr Rech Cancerol, INSERM, UMR S1052, F-69008 Lyon, France
[2] Ctr Rech Cancerol, CNRS, UMR5286, F-69008 Lyon, France
[3] Ctr Rech Cancerol, UNIV UMR1052, F-69008 Lyon, France
[4] Univ Lyon, F-69000 Lyon, France
[5] Ctr Leon Berard, F-69008 Lyon, France
[6] Inst Univ France, F-75000 Paris, France
关键词
EMT; Failsafe program escape; Tumor initiation; EPITHELIAL-MESENCHYMAL TRANSITION; ONCOGENE-INDUCED SENESCENCE; CANCER STEM-CELLS; BREAST-CANCER; E-CADHERIN; CELLULAR SENESCENCE; TWIST EXPRESSION; BLADDER-CANCER; K-RAS; APOPTOSIS;
D O I
10.1016/j.semcancer.2011.09.014
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The epithelial to mesenchymal transition (EMT) is a latent embryonic process which can be aberrantly reactivated during tumor progression. It is generally viewed as one of the main forces driving metastatic dissemination, by providing cells with invasive and motility capabilities. The aberrant reactivation of embryonic EMT inducers has now been additionally linked to escape from senescence and apoptosis, which suggests a role in tumor initiation. This oncogenic potential relies on the ability of EMT inducers to neutralize both the RB and p53 oncosuppressive pathways. RB and p53 have recently been described as key factors in the maintenance of epithelial morphology, which suggests an unexpected and intimate crosstalk between EMT and the corresponding safety programs. In this review, we attempt to understand how these two cell processes are interlinked and might facilitate cell transformation and tumor initiation. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:392 / 396
页数:5
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