Transcriptional activation of cyclooxygenase-2 by tumor suppressor p53 requires nuclear factor-kappaB

V. Benoit, E. De Moraes, N. A. Dar, E. Taranchon, V. Bours, A. Hautefeuille, P. Tanière, A. Chariot, J. Y. Scoazec, C. V. De Moura Gallo, M. P. Merville, P. Hainaut

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Résumé

Overexpression of cyclooxygenase-2 (Cox-2) is thought to exert antiapoptotic effects in cancer. Here we show that the tumor suppressor p53 upregulated Cox-2 in esophageal and colon cancer cell lines by inducing the binding of nuclear factor-kappaB (NF-kappaB) to its response element in the COX-2 promoter. Inhibition of NF-kappaB prevented p53 induction of Cox-2 expression. Cooperation between p53 and NF-kappaB was required for activation of COX-2 promoter in response to daunomycin, a DNA-damaging agent. Pharmacological inhibition of Cox-2 enhanced apoptosis in response to daunomycin, in particular in cells containing active p53. In esophageal cancer, there was a correlation between Cox-2 expression and wild-type TP53 in Barrett's esophagus (BE) and in adenocarcinoma, but not in squamous cell carcinoma (P<0.01). These results suggest that p53 and NF-kappaB cooperate in upregulating Cox-2 expression, promoting cell survival in inflammatory precursor lesions such as BE.

langue originaleAnglais
Pages (de - à)5708-5718
Nombre de pages11
journalOncogene
Volume25
Numéro de publication42
Les DOIs
étatPublié - 21 sept. 2006
Modification externeOui

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