CHEK1 and cancer: Collectively, these observations suggest that SFN up-regulates p21 expression in these two cell lines by a p53-independent mechanism and SFN causes G2/M phase arrest by a ROS-dependent pathway, as supported by the previous studies that elevation of ROS in cancer cells caused accumulation of p21, an increase in expression of Chk1 and decrease in Cdc25C through different mechanisms including activation of Erk and p38 signaling pathways [19, 28, 29].