Fig. 6

Inhibition of Pdgfrβ or Pkcα activity reduces EMT and promotes apoptosis suppressing established Brca1-deficient tumor progression. a, b p18^−/−;Brca1^MGKO tumor cells were transplanted into MFPs of NSG mice and allowed to reach ~ 200 mm³ in size. Mice were then treated with daily i.p. injection of DMSO or PDGFR Inh III at 5 mg/kg (a) and DMSO or Ro-31-8220 at 5 mg/kg (b), respectively. The tumor size was determined and plotted. Data are represented as mean ± SD of four (a) and five (b) tumors in each group. *p < 0.05 between two groups at each time point by Student t test. **p < 0.05 between the group that was at the start of treatment and the group that was treated with PDGFR Inh III for 9 days. c Representative tumors treated with DMSO (three tumors) or PDGFR Inh III (three tumors) for 9 days were analyzed by western blot (left). The indicated protein levels of each lane were quantified and normalized by that of Gapdh (right). Note the increased cleaved caspase 3 and decreased Vim in PDGFR Inh III-treated samples (lanes 4, 5, and 6) in comparison with those in DMSO-treated samples (lanes 1, 2, and 3). d Representative tumors treated with DMSO or PDGFR Inh III for 9 days were analyzed by IHC. The insets show the enlarged cells that are representative