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. Author manuscript; available in PMC: 2011 Feb 14.
Published in final edited form as: Cancer Cell. 2008 Dec 9;14(6):458–470. doi: 10.1016/j.ccr.2008.11.003

Figure 6. Akt sensitizes cells to oxidative stress mediated apoptosis in a FoxO-dependent manner.

Figure 6

A. Akt deficiency exerts resistance to oxidative stress induced apoptosis. DNp53-immortalized WT and Akt1/2 DKO MEFs were treated with increasing concentrations of H2O2 (0.1–1 mM) for 2 h, and apoptosis was quantified by DAPI staining. **, *** p<0.01, 0.001 vs. WT. B. Oxidative stress increases the phosphorylation of Akt and FoxO and reduces the expression of MnSOD. DNp53-immortalized WT and Akt1/2 DKO MEFs were treated with 500 μM H2O2 for 10 min, rinsed and then incubated for 2 h prior to cell lysate preparation. The immunoblot shows levels of phosphorylated Akt (Ser473) and FOXO3a (Ser253), total Akt, FOXO3a, MnSOD, and β-actin as a loading control. C, D. Activation of Akt sensitizes the cells to H2O2-induced cell death. Apoptosis after treatment of Rat1a or Rat1a-mAkt cells with increasing concentrations of H2O2 for 2 h. *, ** p<0.05, 0.01 vs. Rat1a. D. Apoptosis after treatment of Pten+/- or Pten-/- MEFs with increasing concentrations of H2O2 for 2 h. **, *** p<0.01, 0.001 vs. PTEN+/-. All data represent the mean ± S.E.M. of three independent experiments.