Brachyury: A New Player in Promoting Breast Cancer Aggressiveness
Menée in vitro et à partir de données portant sur des patientes atteintes d'un cancer du sein ayant reçu un traitement adjuvant à l'aide de tamoxifène, cette étude met en évidence le rôle joué par une surexpression du gène Brachyury dans la transition épithélio-mésenchymateuse et le processus métastatique
In the United States, breast cancer (BC) in women is the second most frequent cause of death and the second most diagnosed cancer, leading to approximately 230000 new cases of invasive BC and approximately 40000 new deaths a year (1,2). A major unmet need for all BCs is better understanding of what drives invasiveness and metastasis, factors responsible for the lethality of this disease. Epithelial-to-mesenchymal transition (EMT), initially described as a critical process in embryogenesis (3) and wound healing (4–7), has been recognized as a possible trigger for metastatic progression of tumors (4,8,9). This important and sometimes reversible process is associated with loss of cell-to-cell adhesion, increased cell motility and invasive properties, and specific morphogenetic changes (8,10). During EMT, certain epithelial markers, such as E-cadherin, are decreased or lost, whereas mesenchymal markers, such as N-cadherin, vimentin, snail, slug, and twist, are upregulated (4,8,10). The latter three are transcription factors (TFs) that are known to control EMT events associated with cancer progression. Brachyury, first discovered in 1927 (11), is the founding member of the highly conserved T-box TF family, whose members share a common DNA-binding domain of 180 …