Research Article

The Role of Wild-Type p53 in Cisplatin-Induced Chk2 Phosphorylation and the Inhibition of Platinum Resistance with a Chk2 Inhibitor

Figure 6

Application of Chk2 inhibitor in combination with cisplatin greatly inhibited cell growth. A2780 or Caov-3 cells (around 1000 per well) were seeded in 96-well plates for 24 hrs and pretreated with different concentrations of Chk2 inhibitor II C3742 for 30 min. Subsequently, cells were treated with cisplatin at IC50 dose for 1 hr while continuously exposed to Chk2 inhibitor. After drug removal, cells were washed twice with PBS, and then incubated with fresh medium containing Chk2 inhibitor for 5 days. Cytotoxicity assay was performed following company’s protocol of Cell Proliferation Kit I (Roche) and the complete solubilization of the purple formazan crystals was measured. Optical density was read at 600 nm to determine cell quantity.
715469.fig.006a
(a) Cell Model: p53 Wild Type
715469.fig.006b
(b) Cell Model: p53 mutant