untitled
<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd>
<responseDate>2018-01-15T18:33:35Z</responseDate>
<request identifier=oai:HAL:hal-01061363v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request>
<GetRecord>
<record>
<header>
<identifier>oai:HAL:hal-01061363v1</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:IGDR</setSpec>
<setSpec>collection:UNIV-RENNES1</setSpec>
<setSpec>collection:IRSET</setSpec>
<setSpec>collection:INSERM</setSpec>
<setSpec>collection:IRSET-TREC</setSpec>
<setSpec>collection:BIOSIT</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:IRSET-6</setSpec>
<setSpec>collection:UNIV-ANGERS</setSpec>
</header>
<metadata><dc>
<publisher>HAL CCSD</publisher>
<title lang=en>Activation of the MKL1/actin signaling pathway induces hormonal escape in estrogen-responsive breast cancer cell lines.</title>
<creator>Kerdivel, Gwenneg</creator>
<creator>Boudot, Antoine</creator>
<creator>Habauzit, Denis</creator>
<creator>Percevault, Frederic</creator>
<creator>Demay, Florence</creator>
<creator>Pakdel, Farzad</creator>
<creator>Flouriot, Gilles</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>Interactions cellulaires et moléculaires (ICM) ; Université de Rennes 1 (UR1) - IFR140 - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>We thank Pr. Vartiainen and Pr. Prywes for providing plasmids. This work was supported by fellowships from The Région Bretagne, the CNRS, the Inserm, the Ligue Contre le Cancer, the University of Rennes 1, and the European University of Brittany.</contributor>
<description>International audience</description>
<source>ISSN: 0303-7207</source>
<source>EISSN: 0303-7207</source>
<source>Molecular and Cellular Endocrinology</source>
<publisher>Elsevier</publisher>
<identifier>hal-01061363</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01061363</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01061363/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01061363/file/Activationsur the_MKL1actin_Kerdivel_et_al._text_Figures.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01061363</source>
<source>Molecular and Cellular Endocrinology, Elsevier, 2014, 390 (1-2), pp.34-44. 〈10.1016/j.mce.2014.03.009〉</source>
<identifier>DOI : 10.1016/j.mce.2014.03.009</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.mce.2014.03.009</relation>
<identifier>PUBMED : 24721635</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24721635</relation>
<language>en</language>
<subject lang=en>Breast cancer</subject>
<subject lang=en>Cell growth</subject>
<subject lang=en>Estrogen receptor</subject>
<subject lang=en>Hormone resistance</subject>
<subject lang=en>MKL1</subject>
<subject lang=en>Tamoxifen</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Estrogen receptor alpha (ERα) is generally considered to be a good prognostic marker because almost 70% of ERα-positive tumors respond to anti-hormone therapies. Unfortunately, during cancer progression, mammary tumors can escape from estrogen control, resulting in resistance to treatment. In this study, we demonstrate that activation of the actin/megakaryoblastic leukemia 1 (MKL1) signaling pathway promotes the hormonal escape of estrogen-sensitive breast cancer cell lines. The actin/MKL1 signaling pathway is silenced in differentiated ERα-positive breast cancer MCF-7 and T47D cell lines and active in ERα-negative HMT-3522 T4-2 and MDA-MB-231 breast cancer cells, which have undergone epithelial-mesenchymal transition. We showed that MKL1 activation in MCF-7 cells, either by modulating actin dynamics or using MKL1 mutants, down-regulates ERα expression and abolishes E2-dependent cell growth. Interestingly, the constitutively active form of MKL1 represses PR and HER2 expression in these cells and increases the expression of HB-EGF, TGFβ, and amphiregulin growth factors in an E2-independent manner. The resulting expression profile (ER-, PR-, HER2-) typically corresponds to the triple-negative breast cancer expression profile.</description>
<date>2014-06-05</date>
</dc>
</metadata>
</record>
</GetRecord>
</OAI-PMH>
