Abstract
Sulforaphane (SFN) has been revealed to inhibit the growth and induce apoptosis of cancer cells. However, the detailed anticancer effects of SFN on p53‑deficient colon cancer cells has yet to be clearly elucidated. The present study employed p53‑deficient SW480 cells to establish an SFN‑induced in vitro model of apoptosis. The critical events leading to apoptosis were then evaluated in SFN‑treated p53‑deficient SW480 cells, by performing an MTT assay, flow cytometry, western blotting and ELISA. The results demonstrated that SFN at concentrations of 5, 10, 15 and 20 µM induced mitochondria‑associated cell apoptosis, which was further confirmed by disruption of the mitochondrial membrane potential, an increase in the Bax/Bcl‑2 ratio, as well as activation of caspase‑3, ‑7 and ‑9. In addition, SFN‑induced apoptosis was associated with an increase in the generation of reactive oxygen species (ROS), and the activation of extracellular signal‑regulated kinases (Erk) and p38 mitogen‑activated protein kinases. However, SFN did not induce expression of the p53 family member, p73. SFN‑induced apoptosis was subsequently confirmed to be ROS‑dependent and associated with Erk/p38, as the specific inhibitors for ROS, phosphorylated (p)‑Erk and p‑p38, completely or partially attenuated the SFN‑induced reduction in SW480 cell viability. In addition, the results demonstrated that even at the lowest concentrations (5 µM), SFN increased the sensitivity of p53‑proficient HCT‑116 cells to cisplatin. In conclusion, the results suggest that SFN may induce apoptosis in p53‑deficient SW480 cells via p53/p73‑independent and ROS‑Erk/p38‑dependent signaling pathways.