Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1

The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how th...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer cell 2012-12, Vol.22 (6), p.709-724
Hauptverfasser: Ocaña, Oscar H., Córcoles, Rebeca, Fabra, Ángels, Moreno-Bueno, Gema, Acloque, Hervé, Vega, Sonia, Barrallo-Gimeno, Alejandro, Cano, Amparo, Nieto, M. Angela
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 724
container_issue 6
container_start_page 709
container_title Cancer cell
container_volume 22
creator Ocaña, Oscar H.
Córcoles, Rebeca
Fabra, Ángels
Moreno-Bueno, Gema
Acloque, Hervé
Vega, Sonia
Barrallo-Gimeno, Alejandro
Cano, Amparo
Nieto, M. Angela
description The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis. ► Prrx1 is an epithelial-mesenchymal transition inducer in embryos and cancer cells ► Prrx1 cooperates with Twist1 for invasion in embryonic and cancer cells ► Prrx1 loss reverts EMT & induces stemness, both required for metastatic colonization ► High Prrx1 expression associates with good prognosis
doi_str_mv 10.1016/j.ccr.2012.10.012
format Article
fullrecord <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_02912713v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1535610812004424</els_id><sourcerecordid>1239060857</sourcerecordid><originalsourceid>FETCH-LOGICAL-c496t-98a7b1f9e1ea9fca8b0f5c3a038dc09e4ea399d4217d6eb7644842c0fe15672f3</originalsourceid><addsrcrecordid>eNp9UU1v1DAUtBCoLaU_gAvKEQ5Z_OLEscWpWvVL2gqEytnyOs9ar7Lx1k4q2l_fl27pkdO8N5qZwwxjn4EvgIP8vl04lxYVh4r-BcE7dgKqVaWQSr6nuxFNKYGrY_Yx5y0nD7T6iB1XgkwgxQnztzjaPNoxuGIZ-ziEJ7rjUPzG-ykkzMW4QXr2dOaZj_6FudgHgj7YvrzFjIPbPO5sX9wlO-TwEnAzdJPDVPxK6S98Yh-87TOeveIp-3N5cbe8Llc_r26W56vS1VqOpVa2XYPXCGi1d1atuW-csFyoznGNNVqhdVdX0HYS162sa1VXjnuERraVF6fs2yF3Y3uzT2Fn06OJNpjr85WZOV5pqFoQD0DarwftPsX7CfNodiE77Hs7YJyygUpoLrlqWpLCQepSzDmhf8sGbuYpzNbQFGaeYqYIyPPlNX5a77B7c_zrngQ_DgKkQh4CJpNdoCaxo97daLoY_hP_DIfAmdw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1239060857</pqid></control><display><type>article</type><title>Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Elsevier ScienceDirect Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Ocaña, Oscar H. ; Córcoles, Rebeca ; Fabra, Ángels ; Moreno-Bueno, Gema ; Acloque, Hervé ; Vega, Sonia ; Barrallo-Gimeno, Alejandro ; Cano, Amparo ; Nieto, M. Angela</creator><creatorcontrib>Ocaña, Oscar H. ; Córcoles, Rebeca ; Fabra, Ángels ; Moreno-Bueno, Gema ; Acloque, Hervé ; Vega, Sonia ; Barrallo-Gimeno, Alejandro ; Cano, Amparo ; Nieto, M. Angela</creatorcontrib><description>The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis. ► Prrx1 is an epithelial-mesenchymal transition inducer in embryos and cancer cells ► Prrx1 cooperates with Twist1 for invasion in embryonic and cancer cells ► Prrx1 loss reverts EMT &amp; induces stemness, both required for metastatic colonization ► High Prrx1 expression associates with good prognosis</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2012.10.012</identifier><identifier>PMID: 23201163</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Cell Behavior ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Movement - physiology ; Cellular Biology ; Development Biology ; Embryology and Organogenesis ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelial-Mesenchymal Transition - genetics ; Epithelial-Mesenchymal Transition - physiology ; Female ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Homeodomain Proteins - physiology ; Humans ; Life Sciences ; MCF-7 Cells ; Middle Aged ; Neoplasm Metastasis ; Prognosis ; Retrospective Studies ; Stem Cells - metabolism ; Stem Cells - pathology</subject><ispartof>Cancer cell, 2012-12, Vol.22 (6), p.709-724</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-98a7b1f9e1ea9fca8b0f5c3a038dc09e4ea399d4217d6eb7644842c0fe15672f3</citedby><cites>FETCH-LOGICAL-c496t-98a7b1f9e1ea9fca8b0f5c3a038dc09e4ea399d4217d6eb7644842c0fe15672f3</cites><orcidid>0000-0003-4761-1055</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1535610812004424$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23201163$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02912713$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Ocaña, Oscar H.</creatorcontrib><creatorcontrib>Córcoles, Rebeca</creatorcontrib><creatorcontrib>Fabra, Ángels</creatorcontrib><creatorcontrib>Moreno-Bueno, Gema</creatorcontrib><creatorcontrib>Acloque, Hervé</creatorcontrib><creatorcontrib>Vega, Sonia</creatorcontrib><creatorcontrib>Barrallo-Gimeno, Alejandro</creatorcontrib><creatorcontrib>Cano, Amparo</creatorcontrib><creatorcontrib>Nieto, M. Angela</creatorcontrib><title>Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis. ► Prrx1 is an epithelial-mesenchymal transition inducer in embryos and cancer cells ► Prrx1 cooperates with Twist1 for invasion in embryonic and cancer cells ► Prrx1 loss reverts EMT &amp; induces stemness, both required for metastatic colonization ► High Prrx1 expression associates with good prognosis</description><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Cell Behavior</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>Cellular Biology</subject><subject>Development Biology</subject><subject>Embryology and Organogenesis</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Epithelial-Mesenchymal Transition - physiology</subject><subject>Female</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Homeodomain Proteins - physiology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>MCF-7 Cells</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Prognosis</subject><subject>Retrospective Studies</subject><subject>Stem Cells - metabolism</subject><subject>Stem Cells - pathology</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1v1DAUtBCoLaU_gAvKEQ5Z_OLEscWpWvVL2gqEytnyOs9ar7Lx1k4q2l_fl27pkdO8N5qZwwxjn4EvgIP8vl04lxYVh4r-BcE7dgKqVaWQSr6nuxFNKYGrY_Yx5y0nD7T6iB1XgkwgxQnztzjaPNoxuGIZ-ziEJ7rjUPzG-ykkzMW4QXr2dOaZj_6FudgHgj7YvrzFjIPbPO5sX9wlO-TwEnAzdJPDVPxK6S98Yh-87TOeveIp-3N5cbe8Llc_r26W56vS1VqOpVa2XYPXCGi1d1atuW-csFyoznGNNVqhdVdX0HYS162sa1VXjnuERraVF6fs2yF3Y3uzT2Fn06OJNpjr85WZOV5pqFoQD0DarwftPsX7CfNodiE77Hs7YJyygUpoLrlqWpLCQepSzDmhf8sGbuYpzNbQFGaeYqYIyPPlNX5a77B7c_zrngQ_DgKkQh4CJpNdoCaxo97daLoY_hP_DIfAmdw</recordid><startdate>20121211</startdate><enddate>20121211</enddate><creator>Ocaña, Oscar H.</creator><creator>Córcoles, Rebeca</creator><creator>Fabra, Ángels</creator><creator>Moreno-Bueno, Gema</creator><creator>Acloque, Hervé</creator><creator>Vega, Sonia</creator><creator>Barrallo-Gimeno, Alejandro</creator><creator>Cano, Amparo</creator><creator>Nieto, M. Angela</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-4761-1055</orcidid></search><sort><creationdate>20121211</creationdate><title>Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1</title><author>Ocaña, Oscar H. ; Córcoles, Rebeca ; Fabra, Ángels ; Moreno-Bueno, Gema ; Acloque, Hervé ; Vega, Sonia ; Barrallo-Gimeno, Alejandro ; Cano, Amparo ; Nieto, M. Angela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-98a7b1f9e1ea9fca8b0f5c3a038dc09e4ea399d4217d6eb7644842c0fe15672f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer</topic><topic>Cell Behavior</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cellular Biology</topic><topic>Development Biology</topic><topic>Embryology and Organogenesis</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Epithelial-Mesenchymal Transition - physiology</topic><topic>Female</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Homeodomain Proteins - physiology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>MCF-7 Cells</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Prognosis</topic><topic>Retrospective Studies</topic><topic>Stem Cells - metabolism</topic><topic>Stem Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ocaña, Oscar H.</creatorcontrib><creatorcontrib>Córcoles, Rebeca</creatorcontrib><creatorcontrib>Fabra, Ángels</creatorcontrib><creatorcontrib>Moreno-Bueno, Gema</creatorcontrib><creatorcontrib>Acloque, Hervé</creatorcontrib><creatorcontrib>Vega, Sonia</creatorcontrib><creatorcontrib>Barrallo-Gimeno, Alejandro</creatorcontrib><creatorcontrib>Cano, Amparo</creatorcontrib><creatorcontrib>Nieto, M. Angela</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ocaña, Oscar H.</au><au>Córcoles, Rebeca</au><au>Fabra, Ángels</au><au>Moreno-Bueno, Gema</au><au>Acloque, Hervé</au><au>Vega, Sonia</au><au>Barrallo-Gimeno, Alejandro</au><au>Cano, Amparo</au><au>Nieto, M. Angela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2012-12-11</date><risdate>2012</risdate><volume>22</volume><issue>6</issue><spage>709</spage><epage>724</epage><pages>709-724</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>The epithelial-mesenchymal transition (EMT) is required in the embryo for the formation of tissues for which cells originate far from their final destination. Carcinoma cells hijack this program for tumor dissemination. The relevance of the EMT in cancer is still debated because it is unclear how these migratory cells colonize distant tissues to form macrometastases. We show that the homeobox factor Prrx1 is an EMT inducer conferring migratory and invasive properties. The loss of Prrx1 is required for cancer cells to metastasize in vivo, which revert to the epithelial phenotype concomitant with the acquisition of stem cell properties. Thus, unlike the classical EMT transcription factors, Prrx1 uncouples EMT and stemness, and is a biomarker associated with patient survival and lack of metastasis. ► Prrx1 is an epithelial-mesenchymal transition inducer in embryos and cancer cells ► Prrx1 cooperates with Twist1 for invasion in embryonic and cancer cells ► Prrx1 loss reverts EMT &amp; induces stemness, both required for metastatic colonization ► High Prrx1 expression associates with good prognosis</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23201163</pmid><doi>10.1016/j.ccr.2012.10.012</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-4761-1055</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1535-6108
ispartof Cancer cell, 2012-12, Vol.22 (6), p.709-724
issn 1535-6108
1878-3686
language eng
recordid cdi_hal_primary_oai_HAL_hal_02912713v1
source MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals
subjects Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cancer
Cell Behavior
Cell Line, Tumor
Cell Movement - genetics
Cell Movement - physiology
Cellular Biology
Development Biology
Embryology and Organogenesis
Epithelial Cells - metabolism
Epithelial Cells - pathology
Epithelial-Mesenchymal Transition - genetics
Epithelial-Mesenchymal Transition - physiology
Female
Homeodomain Proteins - genetics
Homeodomain Proteins - metabolism
Homeodomain Proteins - physiology
Humans
Life Sciences
MCF-7 Cells
Middle Aged
Neoplasm Metastasis
Prognosis
Retrospective Studies
Stem Cells - metabolism
Stem Cells - pathology
title Metastatic Colonization Requires the Repression of the Epithelial-Mesenchymal Transition Inducer Prrx1
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T17%3A59%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Metastatic%20Colonization%20Requires%20the%20Repression%20of%20the%20Epithelial-Mesenchymal%20Transition%20Inducer%20Prrx1&rft.jtitle=Cancer%20cell&rft.au=Oca%C3%B1a,%20Oscar%C2%A0H.&rft.date=2012-12-11&rft.volume=22&rft.issue=6&rft.spage=709&rft.epage=724&rft.pages=709-724&rft.issn=1535-6108&rft.eissn=1878-3686&rft_id=info:doi/10.1016/j.ccr.2012.10.012&rft_dat=%3Cproquest_hal_p%3E1239060857%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1239060857&rft_id=info:pmid/23201163&rft_els_id=S1535610812004424&rfr_iscdi=true