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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>2018-01-15T18:35:51Z</responseDate> <request identifier=oai:HAL:inserm-00808966v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:inserm-00808966v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:INSERM</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-TREC</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:IRSET-6</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Estrogen represses CXCR7 gene expression by inhibiting the recruitment of NFκB transcription factor at the CXCR7 promoter in breast cancer cells.</title> <creator>Kerdivel, Gwenneg</creator> <creator>Boudot, Antoine</creator> <creator>Pakdel, Farzad</creator> <contributor>TREC : Transcription, Environment and Cancer ; 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> <description>International audience</description> <source>ISSN: 0006-291X</source> <source>EISSN: 1090-2104</source> <source>Biochemical and Biophysical Research Communications</source> <publisher>Elsevier</publisher> <identifier>inserm-00808966</identifier> <identifier>http://www.hal.inserm.fr/inserm-00808966</identifier> <source>http://www.hal.inserm.fr/inserm-00808966</source> <source>Biochemical and Biophysical Research Communications, Elsevier, 2013, 431 (4), pp.729-33. 〈10.1016/j.bbrc.2013.01.050〉</source> <identifier>DOI : 10.1016/j.bbrc.2013.01.050</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bbrc.2013.01.050</relation> <identifier>PUBMED : 23352615</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/23352615</relation> <language>en</language> <subject lang=es>Estrogen</subject> <subject lang=es>Estrogen receptor</subject> <subject lang=es>NFκB</subject> <subject lang=es>CXCR7</subject> <subject lang=es>Breast cancer cells</subject> <subject>[SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Although many studies reported mechanisms involved in the positive regulation of estrogens (E2) target genes, very little is known concerning the repressive effect of E2. In this study, we explored the molecular mechanisms by which E2 regulates CXCR7 expression in breast cancer cells. Our results show that E2-mediated down-regulation of CXCR7 occurs at the transcriptional level as demonstrated using actinomycin D and requires estrogen receptor alpha (ERα). In addition, CXCR7 is a primary ERα-target gene because the effect of E2 does not require the synthesis of an intermediary protein as revealed by the translational inhibitor cycloheximide treatment. Using an inhibitor of the NFκB pathway and chromatin immunoprecipitation assays, we demonstrated that NFκB is necessary for the high expression of CXCR7 gene and is recruited to the proximal promoter of the CXCR7 gene. Interestingly, the chromatin immunoprecipitation analyses also showed that E2-treatment significantly prevented the recruitment of NFκB to the promoter. Altogether, our results demonstrate that E2, through ERα, directly down-regulates CXCR7 expression by interfering with NFκB transcription factor at the promoter level.</description> <date>2013-02-22</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>