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. 2019 Jul 25;18(3):3256–3264. doi: 10.3892/ol.2019.10664

Figure 5.

Figure 5.

Cytotoxic effects of MHY695 are independent of p53. (A) NCM460, HT-29, Caco-2, DLD-1 and HCT116 cells were treated with various concentrations of MHY695. *P<0.05, **P<0.01 and ***P<0.001 vs. the vehicle-treated group. (B) Expression levels of phospho-Akt and cleaved PARP were investigated in NCM460, Caco-2, DLD-1 and HT-29 cells by western blot analysis. Cells were treated with vehicle or MHY695 (25 or 50 µM) for 24 h. (C) Cell viability of p53 wt and p53 null HCT116 cells were investigated by MTT assay. p53 wt or p53 null HCT116 cells were treated with vehicle or MHY695 at the specified concentrations for 24 h. (D) Downstream proteins of the p53-associated apoptosis pathway were investigated by western blot analysis. p53 wt HCT116 cells were treated with vehicle or MHY695 at the specified concentrations for 24 h. MHY695, (Z)-5-(3-ethoxy-4-hydroxybenzylidene)-2-thioxothiazolidin-4-one; wt, wild-type; p-Akt, phospho-protein kinase B; PARP, poly(ADP-ribose) polymerase; PUMA, Bcl-2-binding component 3; Bax, Apoptosis regulator BAX; Bak, Bcl-2 homologous antagonist/killer.