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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Exp Cell Res. 2014 Oct 14;331(1):239–250. doi: 10.1016/j.yexcr.2014.10.002

Figure 5.

Figure 5

The effect of AR inhibition on F7 expression and AR activation on factor VII activity, and a schematic model for AR induction of factor VII. (A) Relative expression of F7 using qRT-PCR in T-47D cell line following treatment with flutamide (FLU) for 48 hours. Expression values are presented relative to the control (CTL) experiments. *, p< 0.01 is for FLU-treated vs. control groups. (B) The effect of AR activation by DHT on FVII in T-47D cell line using Tissue Factor (TF)-FVII activity assay. T-47D cells were treated either with DHT or vehicle control for 48h followed by cell lysate extraction and measurement of TF-FVII activity. The ratio of TF-FVII activity in each cell lysate was calculated relative to that of lysate + exogenous FVII and compared between the DHT-treated and control groups. Error Bars: ± 2SEM. (C) A schematic model for the AR-mediated induction of factor VII in breast cancer. In this model, AR induces FVII expression and leads to an increased activity of FVIIa/TF complex in breast cancer cells, which in turn activates FX to FXa conversion. TF: Tissue Factor, FVII: factor VII, FX: factor X, FXa: activated factor X, red arrows indicate a stimulatory effect.