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• W1978503888 abstract "The identification of transcriptional targets of the tumor suppressor p53 is crucial in understanding mechanisms by which it affects cellular outcomes. Through expression array analysis, we identified cyclooxygenase 2 (Cox-2), whose expression was inducible by wild-type p53 and DNA damage. We also found that p53-induced Cox-2 expression results from p53-mediated activation of the Ras/Raf/MAPK cascade, as demonstrated by suppression of Cox-2 induction in response to p53 by dominant-negative Ras or Raf1 mutants. Furthermore, heparin-binding epidermal growth factor-like growth factor (HB- EGF), a p53 downstream target gene, induced Cox-2 expression, implying that Cox-2 is an ultimate effector in the p53-->HB-EGF-->Ras/Raf/MAPK-->Cox-2 pathway. p53-induced apoptosis was enhanced greatly in Cox-2 knock-out cells as compared with wild-type cells, suggesting that Cox-2 has an abrogating effect on p53-induced apoptosis. Also, a selective Cox-2 inhibitor, NS-398, significantly enhanced genotoxic stress-induced apoptosis in several types of p53+/+ normal human cells, through a caspase-dependent pathway. Together, these results demonstrate that Cox-2 is induced by p53-mediated activation of the Ras/Raf/ERK cascade, counteracting p53-mediated apoptosis. This anti-apoptosis effect may be a mechanism to abate cellular stresses associated with p53 induction." @default.
• W1978503888 created "2016-06-24" @default.
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• W1978503888 date "2002-11-01" @default.
• W1978503888 modified "2023-10-18" @default.
• W1978503888 title "p53-mediated induction of Cox-2 counteracts p53- or genotoxic stress-induced apoptosis" @default.
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• W1978503888 doi "https://doi.org/10.1093/emboj/cdf591" @default.
• W1978503888 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/131088" @default.
• W1978503888 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12411481" @default.
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