GROWTH OF MDA‐MB‐231 CELL LINE: DIFFERENT EFFECTS OF TGF‐β₁, EGF AND ESTRADIOL DEPENDING ON THE LENGTH OF EXPOSURE

Abstract

The human cell line MDA-MB-231 is a prototype for the study of hormone-independent breast cancer. Modification of cell growth behaviour has been observed after treating these cells with growth factors. EGF is a typical stimulatory growth factor for many cell types, whereas transforming growth factor beta(1)(TGF-beta(1)) acts with inhibitory character. Here we observed cell growth inhibition after EGF as well as after TGF-beta(1)treatments. Nevertheless, in the 42-h experiments, EGF-treated cultures grew before (18 hours) respect to the TGF-beta(1)and E(2)-treated cultures (24 h), and in the 11-day experiments, EGF-treated cultures started growing (7 days) after TGF-beta(1)-treated cultures (5 days). Estradiol inhibited the proliferation of these cells only after several days of treatment.

Myeloid Progenitor Cells in the Premetastatic Lung Promote Metastases by Inducing Mesenchymal to Epithelial Transition

“…Versican attenuated the Smad-mediated EMT signaling pathway as determined by the reduction of p-Smad2 levels and suppression of transcription factor Snail. The suppression of Smad2 pathway-induced MET increased cell proliferation consistent with previous reports (40,41). In addition, versican did not impact apoptosis (data not shown), suggesting that versican-mediated stimulation of MET and enhanced proliferation may be the main mechanisms of increased tumor outgrowth and formation of focal macrometastases.…”

Microenvironmental Regulation of Epithelial–Mesenchymal Transitions in Cancer

“…Versican inhibited the TGF-β-Smad2/3 signaling pathway to stimulate MET. Versican-induced MET resulted in increased cell proliferation in agreement with published studies demonstrating that TGF-β inhibits the proliferation of breast cancer lines including MDA-MB-231 by regulating expression of cytostatic genes (40, 41). Consistently, versican-mediated blockade of the TGF-β-Smad2/3 pathway resulted in increased cell proliferation and notably, expression of constitutively activated TGF-β-R1 rescued versican-mediated blockade of TGF-β-Smad2/3 pathway, reversed MET and proliferation, and suppressed metastases.…”

Angiogenesis in breast cancer: The role of transforming growth factor ? and CD105

“…TGF␤s are potent inhibitors of proliferation in normal epithelial cells by inducing cell cycle arrest in late G1 (Alexandrow and Moses, 1995) and apoptosis (Chen et al, 1996). TGF␤1 abolishes the in vitro proliferation of various breast cancer cell lines, such as MCF-7 (Chen et al, 1996), MDA-MB-435 (Yu et al, 1997), MDA-MB-231 (Mur et al, 1998), and Hs578T (Yang et al, 1998).…”