Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells
Fig 6
Cisplatin induces early LMP in HCT-116 p53 -/- cells.
(A) HCT-116 wt and HCT-116 p53-/- cells were treated with cisplatin (20 μM) for 1h. HCT-116 p53 -/- cells were TIRON (10 mM) for 2h and then treated with cisplatin for 1h to examine the effect of TIRON on cisplatin-induced LMP. Cells were stained for galectin-3 to evaluate the lysosomal membrane permeabilization. (B) HCT-116 wt and HCT-116 p53 -/- cells were transfected with BIK siRNA or scrambled siRNA for 24h. Cells were treated with cisplatin (20 μM) or UV (100 mJ/cm2) for 1h and the Cathepsin B/L activity was measured in untransfected and transfected cells (mean RFU±SEM, n = 3). (C) HCT-116 p53 -/- cells were pretreated with CA-074Me (100 μM) or Z-FA-FMK (10 μM) for 2h and then treated with cisplatin (20 μM) or UV (100 mJ/cm2) for 48h. Cell viability was determined by CellTiterGlo assay and expressed as % of untreated control (mean±SEM, n = 3, *P<0.05, **P<0.01).