Mechanical Stress Promotes Cisplatin-Induced Hepatocellular Carcinoma Cell Death

Figure 3

RNA expression of apoptosis-related genes BAX, Caspase-3, XIAP, HSP70, and the internal control β-Actin after exposure of HepG2 cells to different factor(s). Columns from left to right are unstressed cells (negative control), HepG2 cells exposed to UV radiation (positive control), and HepG2 cells exposed to different factor(s). (a) HepG2 cells exposed only to CisPt 2 μg/mL for 24 hours. (b) HepG2 cells cocultured with PBMCs in 3 : 1 ratio (PBMCs : HepG2 cells) for 24 hours. (c) HepG2 cells cocultured with PBMCs in 3 : 1 ratio (PBMCs : HepG2 cells) and simultaneously exposed to CisPt 2 μg/mL for 24 hours. (d) HepG2 cells exposed only to mechanical stress at 300 rpm for 24 hours. (e) HepG2 cells simultaneously exposed to CisPt 2 μg/mL and mechanical stress at 300 rpm for 24 hours. (f) HepG2 cells cocultured with PBMCs in 3 : 1 ratio (PBMCs : HepG2) and simultaneously exposed to mechanical stress at 300 rpm for 24 hours. (g) HepG2 cells cocultured with PBMCs in 3 : 1 ratio (PBMCs : HepG2) and simultaneously exposed to CisPt 2 μg/mL plus mechanical stress at 300 rpm for 24 hours. (h) Caspase-3 RNA levels as indicated by the number of folds relative to the Control. Control = cells not exposed to any factor (negative control), C = CisPt, P = PBMCs, M = mechanical stress, and UV = cells exposed to ultraviolet (positive control). Error bars represent one standard error of the mean.

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