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. 2006 Dec 18;175(6):913–923. doi: 10.1083/jcb.200512100

Figure 8.

Figure 8.

Inhibition of PI3K–Akt pathway enhances drug sensitivity in respiration-deficient cells. (A) Inhibition of Akt phosphorylation by wortmannin in HL60-C6F cells and Raji ρ- clones. Cells were incubated for 24 h with the indicated concentrations of wortmannin (Wortm), and protein extracts were blotted using anti–phospho-Akt (Ser-473 and Thr-308) and anti-Akt antibodies. (B) Inhibition of PI3K–Akt pathway enhanced drug sensitivity in ρ- cells. All five ρ- clones were pretreated with or without wortmannin for 1 h and incubated with 1 μg/ml As2O3 for 24 h. Apoptotic cells were measured by flow cytometry analysis using annexin-V/PI staining. Results are the mean ± the SD of four separate experiments. (C) HL60-C6F cells were pretreated with or without 10 μM wortmannin for 1 h and incubated with 1 μg/ml As2O3 for up to 24 h. Cell lysates were probed for pro–caspase-3 by immunoblotting. A decrease in pro–caspase-3 band intensity indicates its cleavage during apoptosis. (D) Raji ρ- cells (C2) were pretreated with or without 1 μM wortmannin for 1 h, and incubated with 1 μg/ml As2O3 for up to 24 h. Cell lysates were probed for pro–caspase-3 by immunoblotting. (E) Five clones of ρ- cells were pretreated for 1 h with the Akt inhibitor SH-6, as indicated (3–20 μM), and incubated with 1 μg/ml As2O3 for 24 h. Apoptotic cells were then quantified by flow cytometry analysis using annexin-V/PI staining. Results are the mean ± the SD of four separate experiments.