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http://purl.uniprot.org/citations/24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24721635http://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/24721635http://purl.org/dc/terms/identifier"doi:10.1016/j.mce.2014.03.009"xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Flouriot G."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Pakdel F."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Kerdivel G."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Percevault F."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Demay F."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Boudot A."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/author"Habauzit D."xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/name"Mol Cell Endocrinol"xsd:string
http://purl.uniprot.org/citations/24721635http://purl.uniprot.org/core/pages"34-44"xsd:string
http://purl.uniprot.org/citations/24721635http://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/24721635http://purl.uniprot.org/core/volume"390"xsd:string
http://purl.uniprot.org/citations/24721635http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24721635
http://purl.uniprot.org/citations/24721635http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24721635
http://purl.uniprot.org/uniprot/#_B0QY84-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/#_A4FUJ8-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/#_L8E8L9-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/#_Q29R68-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/#_Q969V6-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/#_W0Z7M9-mappedCitation-24721635http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/Q29R68http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24721635
http://purl.uniprot.org/uniprot/B0QY84http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24721635