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Título

A new role of the Rac-GAP ß2-chimaerin in cell adhesion reveals opposite functions in breast cancer initiation and tumor progression

AutorCasado, Victoria ; Barrio-Real, Laura; García-Rostan, Ginesa ; Baumann, Matti; Rocks, Oliver; Caloca, María J.
Palabras claveRac1
E-cadherin
Breast cancer
β2-chimaerin
Metastasis
Fecha de publicación2016
EditorImpact Journals
CitaciónOncotarget 7(19): 28301-28319 (2016)
Resumenβ2-chimaerin is a Rac1-specific negative regulator and a candidate tumor suppressor in breast cancer but its precise function in mammary tumorigenesis in vivo is unknown. Here, we study for the first time the role of β2-chimaerin in breast cancer using a mouse model and describe an unforeseen role for this protein in epithelial cell-cell adhesion. We demonstrate that expression of β2-chimaerin in breast cancer epithelial cells reduces E-cadherin protein levels, thus loosening cell-cell contacts. In vivo, genetic ablation of β2-chimaerin in the MMTV-Neu/ErbB2 mice accelerates tumor onset, but delays tumor progression. Finally, analysis of clinical databases revealed an inverse correlation between β2-chimaerin and E-cadherin gene expressions in Her2+ breast tumors. Furthermore, breast cancer patients with low β2-chimaerin expression have reduced relapse free survival but develop metastasis at similar times. Overall, our data redefine the role of β2-chimaerin as tumor suppressor and provide the first in vivo evidence of a dual function in breast cancer, suppressing tumor initiation but favoring tumor progression.
Versión del editorhttps://doi.org/10.18632/oncotarget.8597
URIhttp://hdl.handle.net/10261/157928
DOI10.18632/oncotarget.8597
Identificadoresdoi: 10.18632/oncotarget.8597
e-issn: 1949-2553
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