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<title lang=en>COUP-TFI modifies CXCL12 and CXCR4 expression by activating EGF signaling and stimulates breast cancer cell migration.</title>
<creator>Boudot, Antoine</creator>
<creator>Kerdivel, Gwenneg</creator>
<creator>Lecomte, Sylvain</creator>
<creator>Flouriot, Gilles</creator>
<creator>Desille, Mireille</creator>
<creator>Godey, Florence</creator>
<creator>Leveque, Jean</creator>
<creator>Tas, Patrick</creator>
<creator>Le Dréan, Yves</creator>
<creator>Pakdel, Farzad</creator>
<contributor>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 )</contributor>
<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>
<contributor>Service de Biologie ; CRLCC Eugène Marquis (CRLCC)</contributor>
<contributor>Foie, métabolismes et cancer ; Université de Rennes 1 (UR1) - 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>This work was supported by La Ligue Contre le Cancer (Grand-ouest, comites 35, 22 et 56), Fond Unique Interministeriel (FUI), La Region de Bretagne, INSERM, CNRS, and the University of Rennes 1.</contributor>
<description>International audience</description>
<source>ISSN: 1471-2407</source>
<source>EISSN: 1471-2407</source>
<source>BMC Cancer</source>
<publisher>BioMed Central</publisher>
<identifier>hal-01024753</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01024753</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01024753/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01024753/file/1471-2407-14-407.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01024753</source>
<source>BMC Cancer, BioMed Central, 2014, 14, pp.407. 〈10.1186/1471-2407-14-407〉</source>
<identifier>DOI : 10.1186/1471-2407-14-407</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1186/1471-2407-14-407</relation>
<identifier>PUBMED : 24906407</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24906407</relation>
<language>en</language>
<subject lang=en>COUP-T</subject>
<subject lang=en>CXCL12 signaling</subject>
<subject lang=en>Estrogen receptor</subject>
<subject lang=en>Cell migration</subject>
<subject lang=en>Breast cancer</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>BACKGROUND: The orphan receptors COUP-TF (chicken ovalbumin upstream promoter transcription factor) I and II are members of the nuclear receptor superfamily that play distinct and critical roles in vertebrate organogenesis. The involvement of COUP-TFs in cancer development has recently been suggested by several studies but remains poorly understood. METHODS: MCF-7 breast cancer cells overexpressing COUP-TFI and human breast tumors were used to investigate the role of COUP-TFI in the regulation of CXCL12/CXCR4 signaling axis in relation to cell growth and migration. We used Immunofluorescence, western-blot, RT-PCR, Formaldehyde-assisted Isolation of Regulatory Elements (FAIRE) assays, as well as cell proliferation and migration assays. RESULTS: Previously, we showed that COUP-TFI expression is enhanced in breast cancer compared to normal tissue. Here, we report that the CXCL12/CXCR4 signaling pathway, a crucial pathway in cell growth and migration, is an endogenous target of COUP-TFI in breast cancer cells. The overexpression of COUP-TFI in MCF-7 cells inhibits the expression of the chemokine CXCL12 and markedly enhances the expression of its receptor, CXCR4. Our results demonstrate that the modification of CXCL12/CXCR4 expression by COUP-TFI is mediated by the activation of epithelial growth factor (EGF) and the EGF receptor. Furthermore, we provide evidence that these effects of COUP-TFI increase the growth and motility of MCF-7 cells in response to CXCL12. Cell migration toward a CXCL12 gradient was inhibited by AMD3100, a specific antagonist of CXCR4, or in the presence of excess CXCL12 in the cell culture medium. The expression profiles of CXCR4, CXCR7, CXCL12, and COUP-TFI mRNA in 82 breast tumors and control non-tumor samples were measured using real-time PCR. CXCR4 expression was found to be significantly increased in the tumors and correlated with the tumor grade, whereas the expression of CXCL12 was significantly decreased in the tumors compared with the healthy samples. Significantly higher COUP-TFI mRNA expression was also detected in grade 1 tumors. CONCLUSIONS: Together, our mechanistic in vitro assays and in vivo results suggest that a reduction in chemokine CXCL12 expression, with an enhancement of CXCR4 expression, provoked by COUP-TFI, could be associated with an increase in the invasive potential of breast cancer cells.</description>
<date>2014</date>
</dc>
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