Epithelial-Mesenchymal Transition and Cell Cooperativity in Metastasis

被引:336
作者
Tsuji, Takanori [2 ]
Ibaragi, Soichiro [3 ]
Hu, Guo-fu [1 ]
机构
[1] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
[2] Beth Israel Deaconess Med Ctr, Dept Radiat Oncol, Boston, MA 02215 USA
[3] Okayama Univ, Grad Sch, Dept Oral & Maxillofacial Surg, Okayama, Japan
基金
美国国家卫生研究院;
关键词
TUMOR PROGRESSION; INVASION; INACTIVATION; METHYLATION; EXPRESSION; INDUCTION; DIVERSITY; GROWTH; EMT;
D O I
10.1158/0008-5472.CAN-09-1618
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The role of epithelial-mesenchymal transition (EMT) in metastasis remains controversial. EMT has been postulated as an absolute requirement for tumor invasion and metastasis. Three different models including incomplete EMT, mesenchymal-epithelial transition (MET), and collective migration have been proposed for the role of EMT in cancer invasion and metastasis. However, skepticism remains about whether EMT truly occurs during cancer progression, and if it does, whether it plays an indispensible role in metastasis. Our recent findings suggest that EMT cells are responsible for degrading the surrounding matrix to enable invasion and intravasation of both EMT and non-EMT cells. Only non-EMT cells that have entered the blood stream are able to re-establish colonies in the secondary sites. Here, we discuss an alternative model for the role of EMT in cancer metastasis in which EMT and non-EMT cells cooperate to complete the entire process of spontaneous metastasis. [Cancer Res 2009;69(18):7135-9]
引用
收藏
页码:7135 / 7139
页数:5
相关论文
共 23 条
[1]   Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence [J].
Ansieau, Stephane ;
Bastid, Jeremy ;
Doreau, Agnes ;
Morel, Anne-Pierre ;
Bouchet, Benjamin P. ;
Thomas, Clemence ;
Fauvet, Frederique ;
Puisieux, Isabelle ;
Doglioni, Claudio ;
Piccinin, Sara ;
Maestro, Roberta ;
Voeltzel, Thibault ;
Selmi, Abdelkader ;
Valsesia-Wittmann, Sandrine ;
de Fromentel, Claude Caron ;
Puisieux, Alain .
CANCER CELL, 2008, 14 (01) :79-89
[2]   A twist code determines the onset of osteoblast differentiation [J].
Bialek, P ;
Kern, B ;
Yang, XL ;
Schrock, M ;
Sosic, D ;
Hong, N ;
Wu, H ;
Yu, K ;
Ornitz, DM ;
Olson, EN ;
Justice, MJ ;
Karsenty, G .
DEVELOPMENTAL CELL, 2004, 6 (03) :423-435
[3]   A "class action" against the microenvironment: do cancer cells cooperate in metastasis? [J].
Bidard, Francois-Clement ;
Pierga, Jean-Yves ;
Vincent-Salomon, Anne ;
Poupon, Marie-France .
CANCER AND METASTASIS REVIEWS, 2008, 27 (01) :5-10
[4]   Reassessing epithelial to mesenchymal transition as a prerequisite for carcinoma invasion and metastasis [J].
Christiansen, Jason J. ;
Rajasekaran, Ayyappan K. .
CANCER RESEARCH, 2006, 66 (17) :8319-8326
[5]   A cluster of noninvoluting endocytic cells at the margin of the zebrafish blastoderm marks the site of embryonic shield formation [J].
Cooper, MS ;
DAmico, LA .
DEVELOPMENTAL BIOLOGY, 1996, 180 (01) :184-198
[6]   Breast cancer progression: Controversies and consensus in the molecular of metastasis and EMT mechanisms [J].
Cowin, Pamela ;
Welch, Danny R. .
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA, 2007, 12 (2-3) :99-102
[7]   Sustained induction of epithelial to mesenchymal transition activates DNA methylation of genes silenced in basal-like breast cancers [J].
Dumont, Nancy ;
Wilson, Matthew B. ;
Crawford, Yongping G. ;
Reynolds, Paul A. ;
Sigaroudinia, Mahvash ;
Tlsty, Thea D. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (39) :14867-14872
[8]   Tumour-cell invasion and migration: Diversity and escape mechanisms [J].
Friedl, P ;
Wolf, K .
NATURE REVIEWS CANCER, 2003, 3 (05) :362-374
[9]   Methylation patterns of the E-cadherin 5′ CpG island are unstable and reflect the dynamic, heterogeneous loss of E-cadherin expression during metastatic progression [J].
Graff, JR ;
Gabrielson, E ;
Fujii, H ;
Baylin, SB ;
Herman, JG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (04) :2727-2732
[10]   Role of p12CDK2-API in transforming growth factor-β1-mediated growth suppression [J].
Hu, MG ;
Hu, GF ;
Kim, Y ;
Tsuji, T ;
McBride, J ;
Hinds, P ;
Wong, DTW .
CANCER RESEARCH, 2004, 64 (02) :490-499