Brembeck, Felix H.

[["dc.bibliographiccitation.firstpage","6770"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","6787"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Zatula, Nathalie"],["dc.contributor.author","Wiese, Maria"],["dc.contributor.author","Bunzendahl, Jens"],["dc.contributor.author","Birchmeier, Walter"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Brembeck, Felix H."],["dc.date.accessioned","2019-07-09T11:42:11Z"],["dc.date.available","2019-07-09T11:42:11Z"],["dc.date.issued","2014-08-30"],["dc.description.abstract","The majority of human breast cancers express estrogen receptor alpha (ER), which is important for therapy with anti-estrogens. Here we describe the role of BCL9-2, a proto-oncogene previously characterized as co-activator of Wnt/ß-catenin signaling, for mammary tumorigenesis in mice and human. ER positive human breast cancers showed overexpression of BCL9-2 and tamoxifen treated patients with high BCL9-2 demonstrated a better survival. BCL9-2 was upregulated during puberty and pregnancy in normal mammary epithelia, but downregulated in the involuted gland. BCL9-2 overexpression in vivo delayed the mammary involution and induced alveolar hyperplasia. Moreover, aged BCL9-2 transgenic mice developed ductal-like mammary tumors with high nuclear ER expression. We found, that primary cell cultures of BCL9-2 breast tumors responded to tamoxifen treatment. Moreover, BCL9-2 regulated the expression of ER and the proliferation of human breast cancer cells independently of ß-catenin. Finally, we describe a novel mechanism, how BCL9-2 regulates ER transcription by interaction with Sp1 through the proximal ESR1 gene promoter. In summary, BCL9-2 induces ER positive breast cancers in vivo, regulates ER expression by a novel ß-catenin independent mechanism in breast cancer cells, and might predict the therapy response to tamoxifen treatment."],["dc.identifier.doi","10.18632/oncotarget.2252"],["dc.identifier.pmid","25149534"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58610"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Breast Neoplasms"],["dc.subject.mesh","Carcinogenesis"],["dc.subject.mesh","DNA-Binding Proteins"],["dc.subject.mesh","Estrogen Receptor alpha"],["dc.subject.mesh","Female"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Mammary Neoplasms, Experimental"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Tamoxifen"],["dc.subject.mesh","Transcription Factors"],["dc.subject.mesh","Transcriptional Activation"],["dc.subject.mesh","Wnt Signaling Pathway"],["dc.subject.mesh","beta Catenin"],["dc.title","The BCL9-2 proto-oncogene governs estrogen receptor alpha expression in breast tumorigenesis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]