Transforming growth factor (TGF)-βinduces an epithelial-to-mesenchymal transition (EMT) in the BRI-JM01 cell line

<p><b>Copyright information:</b></p><p>Taken from "Investigation of three new mouse mammary tumor cell lines as models for transforming growth factor (TGF)-β and Neu pathway signaling studies: identification of a novel model for TGF-β-induced epithelial-to-mesenchymal transition"</p><p>Breast Cancer Research 2004;6(5):R514-R530.</p><p>Published online 6 Jul 2004</p><p>PMCID:PMC549171.</p><p>Copyright © 2004 Lenferink et al.; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.</p> Immunofluorescence microscopy demonstrating the altered localization of E-cadherin, N-cadherin and β-catenin, the rearrangement of F-actin and vimentin filaments, and the disappearance of ZO-1 that accompany the TGF-β1 induced EMT (see text for details). Flow cytometry of nonfixed live cells monitoring the presence of E-cadherin at the cell surface of BRI-JM01 cells that were exposed to TGF-βfor up to 120 hours. Nonspecific isogenic IgG (HA) and cells grown in the absence of TGF-β(CTL) were used as a negative and positive control, respectively. Western blot analysis determining the total cellular content of E-cadherin, N-cadherin and β-catenin in BRI-JM01 cells cultured for 24, 72 and 120 hours in the absence (CTL) or presence of TGF-β(see text for details). BRI-JM01 cells were treated with TGF-βfor 48 hours (BRI-JM01T) and passaged several times in the absence of this growth factor. When seeded in Matrigel these 'TGF-βprimed' BRI-JM01 cells formed larger three-dimensional structures than did the nontreated cells