The nuclear factor-κB and p53 pathways function independently in primary cells and transformed fibroblasts responding to genotoxic damage

With nuclear factor-κB (NF-κB) and p53 functions generally having disparate outcomes for cell survival and cell division, understanding how these pathways are coordinated following a common activation signal such as DNA damage has important implications for cancer therapy. Conflicting reports concerning NF-κB and p53 interplay in different cell line models prompted a reexamination of this issue using mouse primary thymocytes and embryonic fibroblasts, plus fibroblasts transformed by E1A12S. Here, we report that following the treatment of these cells with a range of stress stimuli, p53 and NF-κB were found to regulate cell cycling and survival independently.