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. 2021 Sep 18;22(18):10107. doi: 10.3390/ijms221810107

Figure 2.

Figure 2

PTC596 induces apoptosis in a caspase-dependent manner. (A) Cancer cells (Caki, A549 and HeLa) were treated with PTC596 (1, 5, 10 nM) or PTC209 (10 nM) for 24 h; (B–E) Caki (B–E) and A549 (B) cells were treated with PTC596 (5, 10 nM) for 24 h. Cell death was determined by staining with Annexin V-FITC dye (B). Cell morphology and nuclear condensation were examined using a microscope (C). Fragmentation of the nuclei was examined using a DNA fragmentation assay kit (D). Caspase-3 activity was detected using DEVDase substrate (E); (E,F) Caki cells were pre-treated with z-VAD-fmk (z-VAD, 20 μM) and then treated with PTC596 (10 nM) for 24 h. The sub-G1 population and protein expression were measured by flow cytometry and Western blotting, respectively. The values in graphs (A,B,D–F) represent the mean ± SD of three independent samples. * p < 0.05 compared to the control. # p < 0.05 compared to the treatment of PTC596.