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Oncotarget. 2017 Feb 14;8(7):12052-12066. doi: 10.18632/oncotarget.14511.

Pax-5 is a potent regulator of E-cadherin and breast cancer malignant processes.

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Université de Moncton, Département de chimie et biochimie, Moncton, NB, E1A 3E9, Canada.
Atlantic Cancer Research Institute, Moncton, NB, E1C 8X3, Canada.
Department of Fisheries and Oceans Canada, Molecular Biology Unit, Moncton, NB, E1C 9B6, Canada.
Georges-L.-Dumont University Hospital Centre, Pathology Department, Moncton, NB, E1C 2Z3, Canada.


Pax-5, an essential transcription factor for B lymphocyte development, has been linked with the development and progression of lymphoid cancers and carcinoma. In contrast to B-cell cancer lesions, the specific expression signatures and roles of Pax-5 in breast cancer progression are relatively unknown. In the present study, we set out to profile Pax-5 expression in mammary tissues and elucidate the cellular and molecular roles of Pax-5 in breast cancer processes. Using immunohistology on mammary tissue arrays, Pax-5 was detected in a total of 298/306 (97.6%) samples tested. Interestingly, our studies reveal that Pax-5 inhibits aggressive features and confers anti-proliferative effects in breast carcinoma cells in contrast to its oncogenic properties in B cell cancers. More precisely, Pax-5 suppressed breast cancer cell migration, invasion and tumor spheroid formation while concomitantly promoting cell adhesion properties. We also observed that Pax-5 inhibited and reversed breast cancer epithelial to mesenchymal phenotypic transitioning. Mechanistically, we found that the Pax-5 transcription factor binds and induces gene expression of E-cadherin, a pivotal regulator of epithelialisation. Globally, we demonstrate that Pax-5 is predominant expressed factor in mammary epithelial cells. We also present an important role for Pax-5 in the phenotypic transitioning processes and aggressive features associated with breast cancer malignancy and disease progression.


E-cadherin; EMT-MET; Pax-5; breast cancer; metastasis

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