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Unravelling mechanisms of p53-mediated tumour suppression
Open accessAbstract
p53 is a crucial tumour suppressor that responds to diverse stress signals by orchestrating specific cellular responses, including transient cell cycle arrest, cellular senescence and apoptosis, which are all processes associated with tumour suppression. However, recent studies have challenged the relative importance of these canonical cellular responses for p53-mediated tumour suppression and have highlighted roles for p53 in modulating other cellular processes, including metabolism, stem cell maintenance, invasion and metastasis, as well as communication within the tumour microenvironment. In this Opinion article, we discuss the roles of classical p53 functions, as well as emerging p53-regulated processes, in tumour suppression.
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“Under physiological conditions, the expression of p53 remains low because of the interaction between p53 and MDM2, which promotes p53 proteasome degradation through its E3 ubiquitin ligase activity.52”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [52]
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“Cellular stress, such as DNA damage, hypoxia, and oncogene activation, disturbs the interaction between p53 and MDM2 and inhibits p53 degradation, resulting in p53 accumulation.”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [52]
In the citing paper
“Under normal conditions, cellular p53 protein levels are very low owing to strict control by its negative regulators MDM2 and MDMX, which promote p53 degradation through ubiquitination.27,28”
From Targeting p53 pathways: mechanisms, structures, and advances in therapy (2023) · cites this paper as [27]
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- Post, S. M. et al. p53-dependent senescence delays Eμ-myc-induced B-cell lymphomagenesis. Oncogene 29, 1260–1269 (2010). · DOI
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Targeting Ferroptosis as a Vulnerability in Cancer
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The development of the concept of ferroptosis
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Metadata
- Authors
- Bieging, K. T., Mello, S. S., & Attardi, L. D.
- Venue
- Nature Reviews Cancer
- Published
- 2014-04-17
- Volume
- 14
- Issue
- 5
- Pages
- 359-370
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1966841369
- Cited by
- 1,387
- References
- 53
- FWCI
- 13.09
- Type
- journal article
- Language
- en
- Open access
- green
- Licence
- www.springer.com/tdm (tdm)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Unravelling mechanisms of p53-mediated tumour suppression. https://app.cochat.ai/papers/10.1038/nrc3711
- The paper
- Bieging, K. T., Mello, S. S., & Attardi, L. D. (2014). Unravelling mechanisms of p53-mediated tumour suppression. Nature Reviews Cancer. https://doi.org/10.1038/nrc3711
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.