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. Author manuscript; available in PMC: 2013 Apr 1.
Published in final edited form as: Int J Oncol. 2010 Sep;37(3):541–550. doi: 10.3892/ijo_00000703

Figure 1.

Figure 1

The ER is required for cell survival mediated by signaling through AKT. (A) MCF-7 cells were treated with vehicle control (Con) or E2 (10 nM) in the presence or absence of ICI 182,780 (100 nM) for 24 h and then exposed to TNFα (10 ng/ml). Cells were harvested for CV viability assay 24 h later. Asterisk denotes statistical significance from control (p<0.05). (B) MCF-7 cells were transfected with 2 μg of empty vector (Vec) or constitutive active AKT (AKT-CA) along with pGL3-Luc (200 ng). Cells were treated with vehicle (Con) or ICI 182,780 (100 nM) followed by addition of TNFα (10 ng/ml) for 48 h and harvested for viability assay. Asterisk denotes statistical significance from vector control (p<0.05). All data are the means and standard errors of double treatments from a single experiment, and are representative of at least two independent experiments. (C) MCF-7 cells were transfected with 500 ng of empty vector (Vec) or constitutive active AKT (AKT-CA) along with a pEGFP expression vector (100 ng). Cells were treated with vehicle control (Con) or ICI 182,780 (100 nM), followed by the addition of vehicle or TNF-α (10 ng/ml) and analyzed for cell death by fluorescence microscopy 24 h later.