Figure 3. Restoration of WT p53 function reverses p53^R175H mutant activation of phospho-Met. (A and B) EPC2-hTERT-EGFR-p53^R175H cells treated for 24hrs with 5-iminodaunorubicin (5-ID) in a range from 0.1–10 μM (A), CP-31398 (50 ng/mL–5 μg/mL) (B) show decrease in phospho-Met levels by western blotting; treatment with PRIMA1 (1–10 μM) (B) had no effect in the levels of phopho-Met. (C) Treatment with 5-ID (range 0.1–10 μM) and CP-31398 (range 0.01–10 μg/mL) inhibited cells growth of EPC2-hTERT-EGFR-p53^R175H in WST-1 assay (C). Error bars represent ± SEM, and the Student t test was used to determine significance (*, P ≤ 0.05). (D) Treatment of EPC2-hTERT-EGFR-p53^R175H with 5-ID (1 uM and 5 uM) and CP-31398 (2 ug/mL and 5 ug/mL) caused a decrease in boyden-chamber invasion assay. (C–D) Error bars represent ± SEM, and the Student t test was used to determine significance (*, P ≤ 0.05). (E). H&E staining of organotypic 3D cultures show 5-ID (3 μM) and CP-31398 (5 μg/mL) treatment can reduce invasion, magnification 10×.