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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:33:27Z</responseDate> <request identifier=oai:HAL:hal-00873634v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-00873634v1</identifier> <datestamp>2018-01-11</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:CNRS</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:MARQUIS</setSpec> <setSpec>collection:FNCLCC</setSpec> <setSpec>collection:GAUDUCHEAU</setSpec> <setSpec>collection:ICO</setSpec> <setSpec>collection:UNIV-AMU</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:PAOLI_CALMETTES</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:BERGONIE</setSpec> <setSpec>collection:OSS</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>CD95L cell surface cleavage triggers a pro-metastatic signaling pathway in triple negative breast cancer.</title> <creator>Malleter, Marine</creator> <creator>Tauzin, Sebastien</creator> <creator>Bessede, Alban</creator> <creator>Castellano, Remy</creator> <creator>Goubard, Armelle</creator> <creator>Godey, Florence</creator> <creator>Leveque, Jean</creator> <creator>Jezequel, Pascal</creator> <creator>Campion, Loic</creator> <creator>Campone, Mario</creator> <creator>Ducret, Thomas</creator> <creator>Macgrogan, Gaetan</creator> <creator>Debure, Laure</creator> <creator>Collette, Yves</creator> <creator>Vacher, Pierre</creator> <creator>Legembre, Patrick</creator> <contributor>Récepteur de mort et échappement tumoral ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Centre de Recherche en Cancérologie de Marseille (CRCM) ; Aix Marseille Université (AMU) - Institut Paoli-Calmettes - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)</contributor> <contributor>Institut Paoli Calmettes ; Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)</contributor> <contributor>Service de Biologie ; CRLCC Eugène Marquis (CRLCC)</contributor> <contributor>Département de Biologie Oncologique ; CRLCC René Gauducheau</contributor> <contributor>Centre René Gauducheau ; CRLCC René Gauducheau</contributor> <contributor>Validation et identification de nouvelles cibles en oncologie (VINCO) ; Université Bordeaux Segalen - Bordeaux 2 - Institut Bergonié - CRLCC Bordeaux - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor> <description>International audience</description> <source>ISSN: 0008-5472</source> <source>EISSN: 1538-7445</source> <source>Cancer Research</source> <publisher>American Association for Cancer Research</publisher> <identifier>hal-00873634</identifier> <identifier>https://hal.archives-ouvertes.fr/hal-00873634</identifier> <source>https://hal.archives-ouvertes.fr/hal-00873634</source> <source>Cancer Research, American Association for Cancer Research, 2013, 73 (22), pp.6711-21. 〈10.1158/0008-5472.CAN-13-1794〉</source> <identifier>PUBMED : 24072745</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/24072745</relation> <identifier>DOI : 10.1158/0008-5472.CAN-13-1794</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1158/0008-5472.CAN-13-1794</relation> <language>en</language> <subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Triple-negative breast cancers (TNBC) lacking estrogen and progesterone receptors and HER2 amplification have a relatively high risk of metastatic dissemination, but the mechanistic basis for this risk is not understood. Here we report that serum levels of CD95L are higher in TNBC patients compared to other breast cancer patients. Metalloprotease-mediated cleavage of CD95L expressed by endothelial cells surrounding tumors generates a gradient that promotes cell motility, due to formation of an unconventional CD95-containing receptosome termed the motility-inducing signaling complex. Formation of this complex was instrumental for Nox3-driven ROS generation. Mechanistic investigations revealed a Yes-Orai1-EGFR-PI3K pathway that triggered migration of TNBC cells exposed to CD95L. Our findings establish a pro-metastatic function for metalloprotease-cleaved CD95L in triple-negative breast cancers, revisiting its role in carcinogenesis.</description> <date>2013-09-26</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>