دورية أكاديمية
أعرض في EDS

Pea3 transcription factors and wnt1-induced mouse mammary neoplasia.

التفاصيل البيبلوغرافية
العنوان: Pea3 transcription factors and wnt1-induced mouse mammary neoplasia.
المؤلفون: Baker R; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, New York, USA., Kent CV, Silbermann RA, Hassell JA, Young LJ, Howe LR
المصدر: PloS one [PLoS One] 2010 Jan 22; Vol. 5 (1), pp. e8854. Date of Electronic Publication: 2010 Jan 22.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: Electronic Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Mammary Neoplasms, Experimental/*physiopathology , Transcription Factors/*physiology , Wnt1 Protein/*physiology, Animals ; Base Sequence ; DNA Primers ; Female ; Immunohistochemistry ; Mammary Neoplasms, Experimental/genetics ; Mammary Tumor Virus, Mouse ; Mice ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; TCF Transcription Factors/metabolism ; Transcription Factors/genetics ; Transgenes ; Wnt1 Protein/genetics ; beta Catenin/metabolism
مستخلص: The role of the PEA3 subfamily of Ets transcription factors in breast neoplasia is controversial. Although overexpression of PEA3 (E1AF/ETV4), and of the related factors ERM (ETV5) and ER81 (ETV1), have been observed in human and mouse breast tumors, PEA3 factors have also been ascribed a tumor suppressor function. Here, we utilized the MMTV/Wnt1 mouse strain to further interrogate the role of PEA3 transcription factors in mammary tumorigenesis based on our previous observation that Pea3 is highly expressed in MMTV/Wnt1 mammary tumors. Pea3 expression in mouse mammary tissues was visualized using a Pea3(NLSlacZ) reporter strain. In normal mammary glands, Pea3 expression is predominantly confined to myoepithelial cells. Wnt1 transgene expression induced marked amplification of this cell compartment in nontumorous mammary glands, accompanied by an apparent increase in Pea3 expression. The pattern of Pea3 expression in MMTV/Wnt1 mammary glands recapitulated the cellular profile of activated beta-catenin/TCF signaling, which was visualized using both beta-catenin immunohistochemistry and the beta-catenin/TCF-responsive reporter Axin2(NLSlacZ). To test the requirement for PEA3 factors in Wnt1-induced tumorigenesis, we employed a mammary-targeted dominant negative PEA3 transgene, DeltaNPEA3En. Expression of DeltaNPEA3En delayed early-onset tumor formation in MMTV/Wnt1 virgin females (P = 0.03), suggesting a requirement for PEA3 factor function for Wnt1-driven tumor formation. Consistent with this observation, expression of the DeltaNPEA3En transgene was profoundly reduced in mammary tumors compared to nontumorous mammary glands from bigenic MMTV/Wnt1, MMTV/DeltaNPEA3En mice (P = 0.01). Our data provide the first description of Wnt1-mediated expansion of the Pea3-expressing myoepithelial compartment in nontumorous mammary glands. Consistent with this observation, mammary myoepithelium was selectively responsive to Wnt1. Together these data suggest the MMTV/Wnt1 strain as a potential model of basal breast cancer. Furthermore, this study provides evidence for a protumorigenic role of PEA3 factors in breast neoplasia, and supports targeting the PEA3 transcription factor family in breast cancer.
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معلومات مُعتمدة: R01 CA131219 United States CA NCI NIH HHS; R01 CA131219-02 United States CA NCI NIH HHS
المشرفين على المادة: 0 (DNA Primers)
0 (TCF Transcription Factors)
0 (Transcription Factors)
0 (Wnt1 Protein)
0 (Wnt1 protein, mouse)
0 (beta Catenin)
0 (transcription factor PEA3)
تواريخ الأحداث: Date Created: 20100129 Date Completed: 20100520 Latest Revision: 20211020
رمز التحديث: 20240513
مُعرف محوري في PubMed: PMC2809747
DOI: 10.1371/journal.pone.0008854
PMID: 20107508
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0008854