Journal Article

DKFZ-2017-05736

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice.

Tenhagen, M. ; Klarenbeek, S. ; Braumuller, T. M. ; Hofmann, I.DKFZ* ; van der Groep, P. ; Ter Hoeve, N. ; van der Wall, E. ; Jonkers, J. ; Derksen, P. W. B.

2016
Springer Science + Business Media B.V Dordrecht [u.a.]

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Please use a persistent id in citations: doi:10.1007/s10911-016-9358-3

Abstract: Loss of E-cadherin expression is causal to the development of invasive lobular breast carcinoma (ILC). E-cadherin loss leads to dismantling of the adherens junction and subsequent translocation of p120-catenin (p120) to the cytosol and nucleus. Although p120 is critical for the metastatic potential of ILC through the regulation of Rock-dependent anoikis resistance, it remains unknown whether p120 also contributes to ILC development. Using genetically engineered mouse models with mammary gland-specific inactivation of E-cadherin, p120 and p53, we demonstrate that ILC formation induced by E-cadherin and p53 loss is severely impaired upon concomitant inactivation of p120. Tumors that developed in the triple-knockout mice were mostly basal sarcomatoid carcinomas that displayed overt nuclear atypia and multinucleation. In line with the strong reduction in ILC incidence in triple-knockout mice compared to E-cadherin and p53 double-knockout mice, no functional redundancy of p120 family members was observed in mouse ILC development, as expression and localization of ARVCF, p0071 or δ-catenin was unaltered in ILCs from triple-knockout mice. In conclusion, we show that loss of p120 in the context of the p53-deficient mouse models is dominant over E-cadherin inactivation and its inactivation promotes the development of basal, epithelial-to-mesenchymal-transition (EMT)-type invasive mammary tumors.

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Contributing Institute(s):

1. Vaskuläre Onkologie und Metastasierung (A190)

Research Program(s):

1. 311 - Signalling pathways, cell and tumor biology (POF3-311) (POF3-311)

Appears in the scientific report 2016

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Database coverage:
; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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