p120-catenin is critical for the development of invasive lobular carcinoma in mice
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...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
13 July 2016
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| In: |
Journal of mammary gland biology and neoplasia
Year: 2016, Volume: 21, Issue: 3, Pages: 81-88 |
| ISSN: | 1573-7039 |
| DOI: | 10.1007/s10911-016-9358-3 |
| Online Access: | Verlag, Volltext: https://doi.org/10.1007/s10911-016-9358-3 H5520 |s|Breast cancer, Volltext: https://doi.org/10.1007/s10911-016-9358-3 
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| Author Notes: | Milou Tenhagen, Sjoerd Klarenbeek, Tanya M. Braumuller, Ilse Hofmann, Petra van der Groep, Natalie ter Hoeve, Elsken van der Wall, Jos Jonkers, Patrick W.B. Derksen |
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| 520 | |a 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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