Effect of Antiestrogens on EGF-Mediated Movement of Human Breast Cancer Cells

Abstract

In a previous study we compared the influence of several growth factors on breast cancer cells in culture and observed that epidermal growth factor (EGF) enhanced the invasiveness of estrogen receptor-positive breast cancer cells. The objective of the present study was to determine the influence of three unique antiestrogens on EGF-mediated movement of human breast cancer cells. The rate of movement of MCF-7 breast cancer cells was measured using time-lapse videomicroscopy (TLVM). The MCF-7 cells were pretreated with antiestrogen (either tamoxifen, ICI-182-780 (ICI) or 1,1-dichloro-cis-2,3-diarylcyclopropane (AII)) at 10^–6 mol/l for 4 days, and then treated with EGF (10^–10 mol/l) immediately prior to TLVM. EGF enhanced the motility of the MCF-7 cells at 30–90 min post-administration. However, EGF-mediated motility of the MCF-7 cells was inhibited by antiestrogen pretreatment, with TAM and ICI producing complete inhibition of EGF-induced motility. In conclusion, this study demonstrates that EGF enhances the rate of movement of MCF-7 breast cancer cells and that antiestrogen pretreatment inhibits EGF-mediated motility.

Support of a bi-faceted role of estrogen receptor β (ERβ) in ERα-positive breast cancer cells

“…These properties are in line with evidence that ERβ has a role in cellular adhesion and TGFβ signaling (Alonso-Magdalena, et al 2009; Chang et al 2006; Lindberg et al 2010; Thomas et al 2012). Due to the dual roles of TGFβ in cellular proliferation, cellular migration and cancer metastasis (Bierie and Moses 2009; Buck and Knabbe 2006; Goto, et al 2011; Tong, et al 2002), this aspect of ERβ regulation merits further investigation.…”

Nandrolone and stanozolol upregulate aromatase expression and further increase IGF-I-dependent effects on MCF-7 breast cancer cell proliferation

“…Emerging evidence indicate that androgens mainly exert inhibitory effects on the growth of normal mammary epithelial cells and play a protective role in the pathogenesis of breast cancer (Labrie et al, 2003;Somboonporn and Davis, 2004;Tworoger et al, 2005;Yeh et al, 2003). Nonetheless, there are also some epidemiologic reports supporting the concept that androgens, in certain settings, can contribute to breast cancer growth (Missmer et al, 2004;Tong et al, 2002). These latter effects elicited by androgens can be attributed to their ability to directly activate estrogen receptor (ER)-dependent pathways (Aspinall et al, 2004;Rochefort and Garcia, 1976), as well as to their ability to be converted into estrogens by the aromatase enzyme encoded by the CYP19 gene (Simpson et al, 2000;Sonne-Hansen and Lykkesfeldt, 2005).…”