Cited by 798Telomeres, Telomerase, and SenescenceCancer-related Molecular PathwaysGenetics, Aging, and Longevity in Model Organisms

Senescence and aging: the critical roles of p53

Rufini, A, Tucci, P, Celardo, I, Melino, G·2013·Oncogene

Abstract

p53 functions as a transcription factor involved in cell-cycle control, DNA repair, apoptosis and cellular stress responses. However, besides inducing cell growth arrest and apoptosis, p53 activation also modulates cellular senescence and organismal aging. Senescence is an irreversible cell-cycle arrest that has a crucial role both in aging and as a robust physiological antitumor response, which counteracts oncogenic insults. Therefore, via the regulation of senescence, p53 contributes to tumor growth suppression, in a manner strictly dependent by its expression and cellular context. In this review, we focus on the recent advances on the contribution of p53 to cellular senescence and its implication for cancer therapy, and we will discuss p53's impact on animal lifespan. Moreover, we describe p53-mediated regulation of several physiological pathways that could mediate its role in both senescence and aging.

Integrity signals

Registry

Crossref · 10.1038/onc.2012.640

Cites

48 of 48 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • p53 promotes senescence in response to DNA damage and telomere attrition.

    “p53 also promotes senescence in response to DNA damage and telomere attrition (Rufini et al., 2013).”

    From The Aging Epigenome (2016) · cites this paper as Rufini et al., 2013

  • Too much p53 activity from constitutive activation is detrimental to longevity.

    “too much p53 activity, for example, from constitutive activation, is also detrimental to longevity (reviewed by Rufini et al., 2013).”

    From The Aging Epigenome (2016) · cites this paper as Rufini et al., 2013

  • Another important target of CHEK2 phosphorylation is p53, a critical transcriptional regulator of cellular senescence.

    “Another important target of CHEK2 phosphorylation is p53 [169], a critical transcriptional regulator of cellular senescence [130].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Rufini, A., Tucci, P., Celardo, I., & Melino, G.
Affiliations
  • University of Leicester (GB)
  • University of Rome Tor Vergata (IT)
Corresponding author
Melino, G
Venue
Oncogene
Published
2013-02-18
Volume
32
Issue
43
Pages
5129-5143
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W2009668465
Cited by
798
References
48
Citations by year
2026: 35 · 2025: 45 · 2024: 69 · 2023: 78 · 2022: 82 · 2021: 99 · 2020: 72 · 2019: 65 · 2018: 54 · 2017: 40 · 2016: 45 · 2015: 48 · 2014: 54 · 2013: 12
FWCI
5.73
Type
journal article
Language
en
Open access
closed
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
  • Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
  • Archive of Doctoral Theses and Digital Collections (University of Calabria) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
p53, cellular senescence, biological aging, tumor suppression, antitumor immunity, cancer therapy, lifespan regulation, cell cycle arrest, apoptosis, DNA repair, cellular stress response, transcriptional regulation
MeSH terms
Aging, Cell Cycle, Humans, Neoplasms, Tumor Suppressor Protein p53, Cellular Senescence, Apoptosis

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 ›

Are you an author, or do you see a problem with this page? Request a review