TGF-β switches from tumor suppressor to prometastatic factor in a model of breast cancer progression
J. Clin. Invest. Binwu Tang, et al. 112:1116 doi:10.1172/JCI18899 [Go to this article.]

Figure 1
TGF-β receptor expression and responsiveness in the four human breast epithelial cell lines. (a) Ligand affinity cross-linking. Cell lines were affinity labeled with 100 pM ¹²⁵I-labeled TGF-β1 in the absence (–) or presence (+) of a 50-fold molar excess of unlabeled TGF-β1. The migration positions of the endogenous TGF-β receptors (RI, RII, and RIII) are indicated. MW, molecular weight. (b) Smad phosphorylation and regulation of gene expression. Cells were treated with 2 ng/ml TGF-β and assessed by Western blot analysis for extent of Smad phosphorylation (at t =15 minutes), and effects on fibronectin (FBN) and c-Myc expression (at t = 24 hours). For the c-Myc blot, the arrow indicates the c-Myc band and the filled square indicates a nonspecific band. (c) Growth-inhibitory effects of TGF-β1. Cell proliferation in the presence of increasing amounts of TGF-β1 was quantitated by ³H-thymidine incorporation (incorp.). Results are the means for three determinations normalized to the controls with no added TGF-β for each cell type.