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

With nuclear factor-kappa B (NF-kappa B) 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-kappa B 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 EMUS. Here, we report that following the treatment of these cells with a range of stress stimuli, p53 and NF-kappa B were found to regulate cell cycling and survival independently.