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Fig. 4 | Breast Cancer Research

Fig. 4

From: Acquisition of epithelial-mesenchymal transition phenotype in the tamoxifen-resistant breast cancer cell: a new role for G protein-coupled estrogen receptor in mediating tamoxifen resistance through cancer-associated fibroblast-derived fibronectin and β1-integrin signaling pathway in tumor cells

Fig. 4

β1-integrin silencing restores the tamoxifen sensitivity in MCF-7R cells. (a) The effect of a lentivirus-mediated short hairpin RNA (shRNA) vector targeting β1-integrin was measured by Western blotting in MCF-7R cells. Results are shown as fold-changes in optical density compared with the control (sh/Vec), and normalized to β-actin. *P < 0.05, versus control. Cells were treated with (b) the indicated concentrations of TAM for 108 hours or (c) with therapeutic concentrations of TAM (1 μM) for the indicated time. The data represent means ± standard deviation from three different experiments (a P < 0.05, MCF-7R cells versus MCF-7 cells; b P < 0.05, MCF-7R-sh/Vec versus MCF-7R-sh/ITGB1). (d) Cells were treated with 1 μM TAM and counted after 108 hours. (e) Cell numbers were measured in MCF-7R cells that were left untreated (UN) or pretreated with the specific inhibitory antibody for α2β1-integrin (AK-7; 20 μg/ml) or α5β1-integrin (P1D6; 10 μg/ml) before TAM stimulation. Results are expressed as means ± standard deviation of three independent experiments. *P < 0.05, versus each control. ITGB1, β1-integrin; MCF-7R-sh/ITGB1, MCF-7R cells infected with lentivirus vector targeting β1-integrin; MCF-7R-sh/Vec, MCF-7R cells infected with negative control lentivirus (control); TAM, 4-hydroxytamoxifen

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Breast Cancer Research

ISSN: 1465-542X

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