The epithelial-mesenchymal transition (EMT) phenomenon

被引:338
作者
Savagner, P. [1 ]
机构
[1] CRLC Val dAurelle Paul Lamarque, IRCM INSERM U896, Montpellier, France
关键词
apoptosis; differentiation; epithelium; invasiveness; morphogenesis; E-CADHERIN EXPRESSION; GENE-EXPRESSION; MAMMARY-CARCINOMA; DIFFERENTIAL LOSS; SNAIL; SLUG; TRANSCRIPTION; METASTASIS; CELLS; CARCINOSARCOMA;
D O I
10.1093/annonc/mdq292
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The epithelial-mesenchymal transition (EMT) describes a rapid and often reversible modulation of phenotype by epithelial cells. EMT was originally defined in the context of developmental stages, including heart morphogenesis, mesoderm and neural crest formation. Epithelial cells loosen cell-cell adhesion structures throughout EMT. They modulate their polarity, cytoskeleton organization and typically express vimentin filaments and downregulate cytokeratins. They become isolated, mobile and resistant to anoikis. The EMT at least superficially resembles the evolution from normal to transformed cell phenotype during carcinoma progression. The relevance of the concept of EMT in this context was indicated by in vitro models using transformed epithelial cells. Transduction pathways typical of embryogenic EMT in vivo were also found to be activated during cancer progression. More recently, it has been found that such pathways indicate an increased plasticity linked to cellular stemness and ability to generate tumors. However, in the absence of direct evidence, a number of oncologists and pathologists remain skeptical about applying the EMT concept to human tumor progression. Typically in the cancer field, EMT concept appears to be fully relevant in some situations, but the concept has to be adjusted in other situations to reflect tumor cell renewal and plasticity during carcinoma progression and metastasis.
引用
收藏
页码:89 / 92
页数:4
相关论文
共 42 条
[1]   Slug is overexpressed in gastric carcinomas and may act synergistically with SIPI and Snail in the down-regulation of E-cadherin [J].
Alves, C. Castro ;
Rosivatz, E. ;
Schott, C. ;
Hollweck, R. ;
Becker, I. ;
Sarbia, M. ;
Carneiro, F. ;
Becker, K-F .
JOURNAL OF PATHOLOGY, 2007, 211 (05) :507-515
[2]  
ARNOUX V, 2004, RISE FALL EPITHELIAL, pCH8
[3]   The Snail genes as inducers of cell movement and survival: implications in development and cancer [J].
Barrallo-Gimeno, A ;
Nieto, MA .
DEVELOPMENT, 2005, 132 (14) :3151-3161
[4]   The transcription factor Snail is a repressor of E-cadherin gene expression in epithelial tumour cells [J].
Batlle, E ;
Sancho, E ;
Franci, C ;
Domínguez, D ;
Monfar, M ;
Baulida, J ;
de Herreros, AG .
NATURE CELL BIOLOGY, 2000, 2 (02) :84-89
[5]   Snail is a repressor of RK1P transcription in metastatic prostate cancer cells [J].
Beach, S. ;
Tang, H. ;
Park, S. ;
Dhillon, A. S. ;
Keller, E. T. ;
Kolch, W. ;
Yeung, K. C. .
ONCOGENE, 2008, 27 (15) :2243-2248
[6]  
Berx G, 1996, ONCOGENE, V13, P1919
[7]   Pre-EMTing metastasis?: Recapitulation of morphogenetic processes in cancer [J].
Berx, Geert ;
Raspe, Eric ;
Christofori, Gerhard ;
Thiery, Jean Paul ;
Sleeman, Jonathan P. .
CLINICAL & EXPERIMENTAL METASTASIS, 2007, 24 (08) :587-597
[8]   The transcription factor Slug represses E-cadherin expression and induces epithelial to mesenchymal transitions:: a comparison with Snail and E47 repressors [J].
Bolós, V ;
Peinado, H ;
Pérez-Moreno, MA ;
Fraga, MF ;
Esteller, M ;
Cano, A .
JOURNAL OF CELL SCIENCE, 2003, 116 (03) :499-511
[9]   Overexpression of c-myc induces epithelial mesenchymal transition in mammary epithelial cells [J].
Cho, Kyoung Bin ;
Cho, Min Kyong ;
Lee, Won Young ;
Kang, Keon Wook .
CANCER LETTERS, 2010, 293 (02) :230-239
[10]   Snail and slug play distinct roles during breast carcinoma progression [J].
Come, Christophe ;
Magnino, Fabrice ;
Bibeau, Frederic ;
Barbara, Pascal De Santa ;
Becker, Karl Friedrich ;
Theillet, Charles ;
Savagner, Pierre .
CLINICAL CANCER RESEARCH, 2006, 12 (18) :5395-5402