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. 2015 Jan 21;14(2):232–242. doi: 10.4161/15384101.2014.977096

Figure 5.

Figure 5.

4EGI-1-induced Akt feedback activation counteracts its anticancer effects in vitro. Both MCF7 cells were seeded in 96-well plates. On the second day, they were treated with DMSO, 50 μM 4EGI-1, 0.1 μM MK2206 (A), 5 μM LY294002 (B) or 0.25 μM PP242 (C) individually or in combination for 24, 36 or 48 h. Cell proliferation was determined using the CCK8 assay. Relative proliferation was expressed as fold change vs. the corresponding control (DMSO). All experiments were repeated 3 times. *P < 0 .05, compared to the control. MCF7 cells were treated with DMSO, 50 μM 4EGI-1, 0.1 μM MK2206 (A), 5 μM LY294002 (B) or 0.25 μM PP242 (C) individually or in combination for 12 h and harvested for protein gel blot analysis using indicated antibodies. (D) Control, Rictor or mTOR siRNA transfected MCF7 cells were treated with DMSO or 50 μM 4EGI-1 for 24 and 48 h. Cell proliferation was measured by the CCK8 assay and the cell number was normalized to the corresponding control. The data presented are the mean from 3 independent experiments. *P < 0.05, when compared to the control. For western blot analysis, control, Rictor or mTOR siRNA transfected MCF7 cells were treated with DMSO or 50 μM 4EGI-1 for 12 h and then harvested to prepare whole cell protein lysates.