Figure 2
Addition of myr-p110α into p53fl/fl;KrasG12D double mutants increases PI3K signaling and accelerates mammary tumor initiation with no impact on tumor growth rate. (a) Kaplan–Meier survival curve demonstrating breast tumor onset in the two strains. Log-rank (Mantel–Cox) test was used for statistical analysis. ***P<0.001. (b) Kaplan–Meier survival curve demonstrating mammary tumor progression in each strain. The period of tumor growth was defined as the number of days between when a mammary tumor was first observed in the size range of 12–15 mm2 and when tumor surface area reached the end point of 100 mm2. Log-rank (Mantel–Cox) test was used for statistical analysis. P>0.05, non-significant. (c) Western blot analysis of p110α, p-AKT, AKT and GFP with wild-type (WT) mammary tissue and mammary tumors from p53fl/fl;KrasG12D and p53fl/fl;KrasG12D;myr-p110αwt/fl mice. (d) The graphs of western blot signals of p110α, p-AKT, p-AKT/AKT ratio and AKT quantified and normalized with respect to β-actin. (e) Western blot analysis of p85α, p-PTEN and PTEN with WT mammary tissue and mammary tumors from p53fl/fl;KrasG12D and p53fl/fl;KrasG12D;myr-p110αwt/fl mice. (f) The graphs of western blot signals of p85α, p-PTEN, PTEN and p-PTEN/PTEN ratio quantified and normalized with respect to β-actin. Mean fold increase compared with mammary tissue lysates from a non-Cre harboring age-matched female was calculated after normalization. Error bars are the mean±s.e.m. Two-tailed unpaired Student’s t-test was used for statistical analysis. *P<0.05, **P<0.01 and ***P<0.001. Data in c–f are representative of four independent experiments with biological and technical replicates.
