Tissue Factor Induced by Epithelial-Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells.
Identifieur interne : 001B89 ( PubMed/Corpus ); précédent : 001B88; suivant : 001B90Tissue Factor Induced by Epithelial-Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells.
Auteurs : Morgane Bourcy ; Meggy Suarez-Carmona ; Justine Lambert ; Marie-Emilie Francart ; Hélène Schroeder ; Céline Delierneux ; Nicolas Skrypek ; Erik W. Thompson ; Guy Jérusalem ; Geert Berx ; Marc Thiry ; Silvia Blacher ; Brett G. Hollier ; Agnès Noël ; Cécile Oury ; Myriam Polette ; Christine GillesSource :
- Cancer research [ 1538-7445 ] ; 2016.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Thromboplastin.
- pathology : Neoplastic Cells, Circulating.
- chemical , physiology : Zinc Finger E-box-Binding Homeobox 1.
- secondary : Lung Neoplasms.
- Animals, Blood Coagulation, Cell Line, Tumor, Epithelial-Mesenchymal Transition, Female, Humans, Mice, Mice, Inbred BALB C.
Abstract
Epithelial-mesenchymal transition (EMT) is prominent in circulating tumor cells (CTC), but how it influences metastatic spread in this setting is obscure. Insofar as blood provides a specific microenvironment for tumor cells, we explored a potential link between EMT and coagulation that may provide EMT-positive CTCs with enhanced colonizing properties. Here we report that EMT induces tissue factor (TF), a major cell-associated initiator of coagulation and related procoagulant properties in the blood. TF blockade by antibody or shRNA diminished the procoagulant activity of EMT-positive cells, confirming a functional role for TF in these processes. Silencing the EMT transcription factor ZEB1 inhibited both EMT-associated TF expression and coagulant activity, further strengthening the link between EMT and coagulation. Accordingly, EMT-positive cells exhibited a higher persistance/survival in the lungs of mice colonized after intravenous injection, a feature diminished by TF or ZEB1 silencing. In tumor cells with limited metastatic capability, enforcing expression of the EMT transcription factor Snail increased TF, coagulant properties, and early metastasis. Clinically, we identified a subpopulation of CTC expressing vimentin and TF in the blood of metastatic breast cancer patients consistent with our observations. Overall, our findings define a novel EMT-TF regulatory axis that triggers local activation of coagulation pathways to support metastatic colonization of EMT-positive CTCs. Cancer Res; 76(14); 4270-82. ©2016 AACR.
DOI: 10.1158/0008-5472.CAN-15-2263
PubMed: 27221703
Links to Exploration step
pubmed:27221703Le document en format XML
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<author><name sortKey="Thompson, Erik W" sort="Thompson, Erik W" uniqKey="Thompson E" first="Erik W" last="Thompson">Erik W. Thompson</name>
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<author><name sortKey="Berx, Geert" sort="Berx, Geert" uniqKey="Berx G" first="Geert" last="Berx">Geert Berx</name>
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<author><name sortKey="Polette, Myriam" sort="Polette, Myriam" uniqKey="Polette M" first="Myriam" last="Polette">Myriam Polette</name>
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<term>Blood Coagulation</term>
<term>Cell Line, Tumor</term>
<term>Epithelial-Mesenchymal Transition</term>
<term>Female</term>
<term>Humans</term>
<term>Lung Neoplasms (secondary)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Neoplastic Cells, Circulating (pathology)</term>
<term>Thromboplastin (biosynthesis)</term>
<term>Zinc Finger E-box-Binding Homeobox 1 (physiology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Thromboplastin</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplastic Cells, Circulating</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Zinc Finger E-box-Binding Homeobox 1</term>
</keywords>
<keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Blood Coagulation</term>
<term>Cell Line, Tumor</term>
<term>Epithelial-Mesenchymal Transition</term>
<term>Female</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Epithelial-mesenchymal transition (EMT) is prominent in circulating tumor cells (CTC), but how it influences metastatic spread in this setting is obscure. Insofar as blood provides a specific microenvironment for tumor cells, we explored a potential link between EMT and coagulation that may provide EMT-positive CTCs with enhanced colonizing properties. Here we report that EMT induces tissue factor (TF), a major cell-associated initiator of coagulation and related procoagulant properties in the blood. TF blockade by antibody or shRNA diminished the procoagulant activity of EMT-positive cells, confirming a functional role for TF in these processes. Silencing the EMT transcription factor ZEB1 inhibited both EMT-associated TF expression and coagulant activity, further strengthening the link between EMT and coagulation. Accordingly, EMT-positive cells exhibited a higher persistance/survival in the lungs of mice colonized after intravenous injection, a feature diminished by TF or ZEB1 silencing. In tumor cells with limited metastatic capability, enforcing expression of the EMT transcription factor Snail increased TF, coagulant properties, and early metastasis. Clinically, we identified a subpopulation of CTC expressing vimentin and TF in the blood of metastatic breast cancer patients consistent with our observations. Overall, our findings define a novel EMT-TF regulatory axis that triggers local activation of coagulation pathways to support metastatic colonization of EMT-positive CTCs. Cancer Res; 76(14); 4270-82. ©2016 AACR.</div>
</front>
</TEI>
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<Month>09</Month>
<Day>22</Day>
</DateCreated>
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<Month>07</Month>
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<Title>Cancer research</Title>
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<ArticleTitle>Tissue Factor Induced by Epithelial-Mesenchymal Transition Triggers a Procoagulant State That Drives Metastasis of Circulating Tumor Cells.</ArticleTitle>
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<ELocationID EIdType="doi" ValidYN="Y">10.1158/0008-5472.CAN-15-2263</ELocationID>
<Abstract><AbstractText>Epithelial-mesenchymal transition (EMT) is prominent in circulating tumor cells (CTC), but how it influences metastatic spread in this setting is obscure. Insofar as blood provides a specific microenvironment for tumor cells, we explored a potential link between EMT and coagulation that may provide EMT-positive CTCs with enhanced colonizing properties. Here we report that EMT induces tissue factor (TF), a major cell-associated initiator of coagulation and related procoagulant properties in the blood. TF blockade by antibody or shRNA diminished the procoagulant activity of EMT-positive cells, confirming a functional role for TF in these processes. Silencing the EMT transcription factor ZEB1 inhibited both EMT-associated TF expression and coagulant activity, further strengthening the link between EMT and coagulation. Accordingly, EMT-positive cells exhibited a higher persistance/survival in the lungs of mice colonized after intravenous injection, a feature diminished by TF or ZEB1 silencing. In tumor cells with limited metastatic capability, enforcing expression of the EMT transcription factor Snail increased TF, coagulant properties, and early metastasis. Clinically, we identified a subpopulation of CTC expressing vimentin and TF in the blood of metastatic breast cancer patients consistent with our observations. Overall, our findings define a novel EMT-TF regulatory axis that triggers local activation of coagulation pathways to support metastatic colonization of EMT-positive CTCs. Cancer Res; 76(14); 4270-82. ©2016 AACR.</AbstractText>
<CopyrightInformation>©2016 American Association for Cancer Research.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bourcy</LastName>
<ForeName>Morgane</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>GIGA-Cancer, Laboratory of Tumor and Development Biology, University of Liège, Liège, Belgium.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Suarez-Carmona</LastName>
<ForeName>Meggy</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>GIGA-Cancer, Laboratory of Tumor and Development Biology, University of Liège, Liège, Belgium.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Lambert</LastName>
<ForeName>Justine</ForeName>
<Initials>J</Initials>
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<ForeName>Céline</ForeName>
<Initials>C</Initials>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Skrypek</LastName>
<ForeName>Nicolas</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Unit of Molecular and Cellular Oncology Lab, Inflammation Research Center, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Cancer Research Institute Ghent (CRIG), Ghent University, Ghent, Belgium.</Affiliation>
</AffiliationInfo>
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<ForeName>Erik W</ForeName>
<Initials>EW</Initials>
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<ForeName>Guy</ForeName>
<Initials>G</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berx</LastName>
<ForeName>Geert</ForeName>
<Initials>G</Initials>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Thiry</LastName>
<ForeName>Marc</ForeName>
<Initials>M</Initials>
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<ForeName>Silvia</ForeName>
<Initials>S</Initials>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Hollier</LastName>
<ForeName>Brett G</ForeName>
<Initials>BG</Initials>
<AffiliationInfo><Affiliation>Australian Prostate Cancer Research Centre - Queensland, Institute of Health and Biomedical Innovation, School of Biomedical Sciences, Queensland University of Technology, Princess Alexandra Hospital, Translational Research Institute, Brisbane, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Noël</LastName>
<ForeName>Agnès</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>GIGA-Cancer, Laboratory of Tumor and Development Biology, University of Liège, Liège, Belgium.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Oury</LastName>
<ForeName>Cécile</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>GIGA-Cardiovascular Sciences, Laboratory of Thrombosis and Hemostasis, University of Liège, Liège, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Polette</LastName>
<ForeName>Myriam</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>INSERM UMR-S 903, CHU, Biopathology Laboratory, University of Reims, Reims, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gilles</LastName>
<ForeName>Christine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>GIGA-Cancer, Laboratory of Tumor and Development Biology, University of Liège, Liège, Belgium. cgilles@ulg.ac.be.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Month>05</Month>
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