Epithelial-mesenchymal plasticity and circulating tumor cells: Travel companions to metastases

被引：80

作者：

Francart, Marie-Emilie ^{[1
]}

Lambert, Justine ^{[1
]}

Vanwynsberghe, Aline M. ^{[1
]}

Thompson, Erik W. ^{[2
,3
,4
,5
]}

Bourcy, Morgane ^{[1
]}

Polette, Myriam ^{[6
]}

Gilles, Christine ^{[1
]}

机构：

[1] Univ Liege, Lab Tumor & Dev Biol, GIGA Canc, Liege, Belgium

[2] Queensland Univ Technol, Inst Hlth & Biomed Innovat, Brisbane, Qld, Australia

[3] Queensland Univ Technol, Sch Biomed Sci, Brisbane, Qld, Australia

[4] Translat Res Inst Brisbane, Brisbane, Qld, Australia

[5] Univ Melbourne, St Vincents Hosp, Dept Surg, Melbourne, Vic, Australia

[6] Univ Reims, CHU Reims, Biopathol Lab, Inserm,UMR S 903, Reims, France

来源：

DEVELOPMENTAL DYNAMICS | 2018年 / 247卷 / 03期

关键词：

EMT; EMP; CTC; early metastasis; coagulation; BREAST-CANCER PATIENTS; GROWTH-FACTOR RECEPTOR; BETA SIGNALING SWITCHES; TISSUE FACTOR; LUNG-CANCER; E-CADHERIN; PROCOAGULANT FUNCTION; HEMOSTATIC FACTORS; ADVANCED PROSTATE; PERIPHERAL-BLOOD;

D O I：

10.1002/dvdy.24506

中图分类号：

R602 [外科病理学、解剖学]; R32 [人体形态学];

学科分类号：

100101 ;

摘要：

Epithelial-mesenchymal transitions (EMTs) associated with metastatic progression may contribute to the generation of hybrid phenotypes capable of plasticity. This cellular plasticity would provide tumor cells with an increased potential to adapt to the different microenvironments encountered during metastatic spread. Understanding how EMT may functionally equip circulating tumor cells (CTCs) with an enhanced competence to survive in the bloodstream and niche in the colonized organs has thus become a major cancer research axis. We summarize here clinical data with CTC endpoints involving EMT. We then review the work functionally linking EMT programs to CTC biology and deciphering molecular EMT-driven mechanisms supporting their metastatic competence. Developmental Dynamics 247:432-450, 2018. (c) 2017 Wiley Periodicals, Inc.

引用

页码：432 / 450

页数：19

共 216 条

[51] Regulatory networks defining EMT during cancer initiation and progression [J].

De Craene, Bram ;

Berx, Geert .

NATURE REVIEWS CANCER, 2013, 13 (02) :97-110

[52] Hemostatic factors, innate immunity and malignancy [J].

Degen, Jay L. ;

Palumbo, Joseph S. .

THROMBOSIS RESEARCH, 2012, 129 :S1-S5

[53] The molecular composition of the metastatic niche [J].

Descot, Arnaud ;

Oskarsson, Thordur .

EXPERIMENTAL CELL RESEARCH, 2013, 319 (11) :1679-1686

[54] Epithelial-mesenchymal transition (EMT) and metastasis: yes, no, maybe? [J].

Diepenbruck, Maren ;

Christofori, Gerhard .

CURRENT OPINION IN CELL BIOLOGY, 2016, 43 :7-13

[55] ZEB1 Enhances Transendothelial Migration and Represses the Epithelial Phenotype of Prostate Cancer Cells [J].

Drake, Justin M. ;

Strohbehn, Garth ;

Bair, Thomas B. ;

Moreland, Jessica G. ;

Henry, Michael D. .

MOLECULAR BIOLOGY OF THE CELL, 2009, 20 (08) :2207-2217

[56] Targeting Epithelial-Mesenchymal Transition (EMT) to Overcome Drug Resistance in Cancer [J].

Du, Bowen ;

Shim, Joong Sup .

MOLECULES, 2016, 21 (07)

[57] Malignant cells facilitate lung metastasis by bringing their own soil [J].

Duda, Dan G. ;

Duyverman, Annique M. M. J. ;

Kohno, Mitsutomo ;

Snuderl, Matija ;

Steller, Ernst J. A. ;

Fukumura, Dai ;

Jain, Rakesh K. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (50) :21677-21682

[58]

Escrivà M, 2008, MOL CELL BIOL, V28, P1528, DOI 10.1128/MCB.02061-07

[59] New Insights into the Crossroads between EMT and Stemness in the Context of Cancer [J].

Fabregat, Isabel ;

Malfettone, Andrea ;

Soukupova, Jitka .

JOURNAL OF CLINICAL MEDICINE, 2016, 5 (03)

[60]

FIDLER IJ, 1973, EUR J CANCER, V9, P223, DOI 10.1016/S0014-2964(73)80022-2

← 1 2 3 4 5 6 7 8 9 10 →