Additive effect between NF-κB subunits and p53 protein for transcriptional activation of human p53 promoter

Benoît, Valérie; Hellin, Anne-Cécile; Huygen, Sandra; Gielen, Jacques; Bours, Vincent; Merville, Marie‐Paule

doi:10.1038/sj.onc.1203831

Cited by 45 publications

(34 citation statements)

References 48 publications

(44 reference statements)

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“…Recent work suggests the involvement of p53 promoter activation by NF-kB (Benoit et al, 2000) and the existence of a promoter element that is involved in basal p53 gene expression and the stress response (Noda et al, 2000). Thus, suppression of NF-kB in cancer cells may provide an additional target for prevention of cancer.…”

Section: Discussionmentioning

confidence: 99%

Crosstalk between PARP-1 and NF-κB modulates the promotion of skin neoplasia

et al. 2004

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Poly (ADP-ribose) polymerase-1 (PARP-1)-deficient mice are protected against septic shock, type I diabetes, stroke and inflammation. It is now accepted that inflammation and related events, such as activation of NF-jB, are key components in the initiation and progression of epithelial cancer and in particular in the neoplastic transformation of keratinocytes and skin carcinogenesis. Here, we report that PARP-1-deficient mice display a strikingly reduced susceptibility to skin carcinogenesis. In parp-1 À/À mice, development of papilloma-like premalignant lesions induced with DMBA and TPA, is strongly delayed and the final number of tumorbearing mice and total tumor number were significantly reduced. In addition, epidermis of parp-1 À/À mice did not show increased proliferation rates after treatment with carcinogen. Deregulated NF-jB is a hallmark for tumorigenesis together with the concomitant release of early inflammatory mediators. In the absence of PARP-1, NF-jB activation and induction jB-target genes did not take place during the promotion of tumor development. These results suggest that PARP-1 abolition impairs the promotion of skin carcinogenesis interfering with the activation of NF-jB and might have an important implication in targeting PARP-1 as a new antineoplastic therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Crosstalk between PARP-1 and NF-κB modulates the promotion of skin neoplasia

et al. 2004

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“…In contrast, Ryan et al (2000) reported that induction of p53 caused activation of NF-kappaB and that this phenomenon correlated with the ability of p53 to induce apoptosis (Ryan et al, 2000). We previously showed an additive effect between NF-kappaB subunits and p53 for the transcriptional activation of TP53 (Benoit et al, 2000). Bohuslav et al (2004) described that p53 expression stimulated the S6 ribosomal serine/threonine kinase (RSK1), which in turn phosphorylated and activated the p65/RelA subunit of NF-kappaB (Bohuslav et al, 2004).…”

Section: Mechanisms Of P53-nuclear Factor-kappab Cooperationmentioning

confidence: 99%

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

et al. 2006

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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 DNAdamaging 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 (Po0.01). These results suggest that p53 and NF-kappaB cooperate in upregulating Cox-2 expression, promoting cell survival in inflammatory precursor lesions such as BE.

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“…Compared to the vast information and knowledge available regarding the regulation of p53 protein expression and function (Wang and Friedman, 2000;Ito et al, 2001;Wang et al, 2001), there is only a small amount of literature on transcriptional regulation of the p53 gene (Balint and Reisman, 1996;Benoit et al, 2000;Mokdad-Gargouri et al, 2001). However, control of p53 gene expression at the transcriptional level has been shown to play important roles in mitogenic stimulation or factor induced di erentiation (Reich and Levine, 1984;Soini et al, 1992;).…”

Section: Introductionmentioning

confidence: 99%

“…The transcription factors shown to positively regulate p53 transcription include c-myc (Kirch et al, 1999;Lee and Rho, 2000), NF-kB (Pei et al, 1999;Benoit et al, 2000), YY1/NF1 (Lee et al, 1998(Lee et al, , 1999Nayak and Das, 1999), Ap1 (Kirch et al, 1999), and the HoxA5 homeobox containing gene product (Raman et al, 2000). Members of the PAX family are the only mammalian nuclear proteins shown to repress p53 transcription through a binding site present in the ®rst non-coding exon (Stuart et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

The critical role of the PE21 element in oncostatin M-mediated transcriptional repression of the p53 tumor suppressor gene in breast cancer cells

et al. 2001

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Cytokine oncostatin M (OM) exerts growth-inhibitory and di erentiative e ects on breast cancer cells. Previously we showed that the transcription from the p53 gene in breast cancer cells was down regulated by OM. To elucidate the molecular mechanisms underlying the OM e ect on p53 transcription, in this study, we dissected the p53 promoter region and analysed the p53 promoter activity in breast tumor cells. We showed that treatment of MCF-7 cells with OM induced a dose-and time-dependent suppression of p53 promoter activity. The p53 promoter activity was decreased to 35% of control at 24 h and further decreased to 20% at 48 h by OM at concentrations of 5 ng/ml and higher. Deletion of the 5'-¯anking region of the p53 promoter from 7426 to 797 did not a ect the OM e ect. However, further deletion to 740 completely abolished the repressive e ect of OM. The p53 promoter region 796 to 741 contains NF-kB and c-myc binding sites, and a newly identi®ed UV-inducible element PE21. Mutations to disrupt NF-kB binding or c-myc binding to the p53 promoter decreased the basal promoter activity without a ecting the OM-mediated suppression, whereas mutation at the PE21 motif totally abolished the OM e ect. We further demonstrated that insertion of PE21 element upstream of the thymidine kinase minimal promoter generated an OM response analogous to that of the p53 promoter. Finally, we detected the speci®c binding of a nuclear protein with a molecular mass of 87 kDa to the PE21 motif. Taken together, we demonstrate that OM inhibits the transcription of the p53 gene through the PE21 element. Thus, the PE21 element is functionally involved in p53 transcription regulated by UV-induction and OM suppression. Oncogene (2001) 20, 8193 ± 8202.

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Additive effect between NF-κB subunits and p53 protein for transcriptional activation of human p53 promoter

Cited by 45 publications

References 48 publications

Crosstalk between PARP-1 and NF-κB modulates the promotion of skin neoplasia

Crosstalk between PARP-1 and NF-κB modulates the promotion of skin neoplasia

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

The critical role of the PE21 element in oncostatin M-mediated transcriptional repression of the p53 tumor suppressor gene in breast cancer cells

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