http://purl.uniprot.org/citations/24721635 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24721635 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.mce.2014.03.009"xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Flouriot G."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Pakdel F."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Kerdivel G."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Percevault F."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Demay F."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Boudot A."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/author | "Habauzit D."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/name | "Mol Cell Endocrinol"xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/pages | "34-44"xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/title | "Activation of the MKL1/actin signaling pathway induces hormonal escape in estrogen-responsive breast cancer cell lines."xsd:string |
http://purl.uniprot.org/citations/24721635 | http://purl.uniprot.org/core/volume | "390"xsd:string |
http://purl.uniprot.org/citations/24721635 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24721635 |
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