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. 2002 Apr 15;16(8):984–993. doi: 10.1101/gad.973602

Figure 5.

Figure 5

(A) Western blot analysis of cell lines exposed to 200J of ultraviolet irradiation (UV). In A549, with wild-type p53 and intact PTEN protein expression, UV exposure resulted in increased p53 protein expression and related increase in PTEN and decrease in PI3K p110α and phosphorylated AKT levels. In cell line MDA886, containing wild-type p53 and no PTEN protein expression, UV exposure resulted in a decrease in PI3K p110α and phosphorylated AKT protein levels. In cell line H157, containing mutated p53 and PTEN, UV irradiation had no effects on PI3K p110α, or AKT protein levels. (B,C) Synergism analysis between p53 induction and PI3K inhibition in cell line A549 showing cell viability (B) and isobologram (C). Synergism was identified at all dose levels. (D,E) Synergism analysis in cell line MDA 886. Synergism was detected in a dose dependent manner and to a greater extent than in cell line A549. (F,G) Transfection of myrPIK3CA into MDA886 results in resistance to p53-related apoptosis, as shown in growth curve F and abrogates p53-related decrease in phosphorylated AKT compared to null vector detected by Western blotting (G). Transfection of asPIK3CA into MDA886 cells resulted in rapid cell death and increased sensitivity to UV irradiation (F).