The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
p53 Suppresses the Nrf2-dependent Transcription of Antioxidant Response Genes
Open accessAbstract
Cells respond to the shift of intracellular environment toward pro-oxidant conditions by activating the transcription of numerous "antioxidant" genes. This response is based on the activation of the Nrf2 transcription factor, which transactivates the genes containing in their promoters the antioxidant response cis-elements (AREs). If the oxidative stress provokes DNA damage, a second response of the cell takes place, based on the activation of p53, which induces cell cycle arrest and/or apoptosis. Here we have explored the cross-talk between these two regulatory mechanisms. The results show that p53 counteracts the Nrf2-induced transcription of three ARE-containing promoters of the x-CT, NQO1, and GST-alpha1 genes. Endogenous transcripts of these antioxidant genes accumulate as a consequence of Nrf2 overexpression or exposure to electrophile diethylmaleate, but these effects are again blocked by p53 overexpression or endogenous p53 activation. Chromatin immunoprecipitation experiments support the hypothesis that this p53-dependent trans-repression is due to the direct interaction of p53 with the ARE-containing promoters. Considering that p53-induced apoptosis requires an accumulation of reactive oxygen species, this negative control on the Nrf2 transactivation appears to be aimed to prevent the generation of a strong anti-oxidant intracellular environment that could hinder the induction of apoptosis.
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Cites
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A model for p53-induced apoptosis
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Suppression of Human Colorectal Carcinoma Cell Growth by Wild-Type p53
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Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex
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Cited by
Hayes, J. D., Dinkova-Kostova, A. T., & Tew, K. D. (2020) · Cancer Cell · doi:10.1016/j.ccell.2020.06.001 · Cited by 2,654
ROS and the DNA damage response in cancer
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“Decreased Keap1-Nrf2 interaction [111,112] and loss-of-function mutations of Keap1 [112,113] lead to aberrant Nrf2 activation, and therefore resistance to radiotherapy.”
BackgroundInfluentialRedox regulation of cell survival
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NRF2 and the Hallmarks of Cancer
Rojo de la Vega, M., Chapman, E., & Zhang, D. D. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.022 · Cited by 1,672
P53 in survival, death and metabolic health: a lifeguard with a licence to kill.
Kruiswijk, F., Labuschagne, C. F., & Vousden, K. H. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm4007 · Cited by 1,080
Metadata
- Authors
- Faraonio, R., Vergara, P., Di Marzo, D., Pierantoni, M. G., Napolitano, M., Russo, T., & Cimino, F.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2006-12
- Volume
- 281
- Issue
- 52
- Pages
- 39776-39784
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1964190328
- Cited by
- 349
- References
- 33
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
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