Cited by 1,222Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

The Cell–Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression

Open access
Chen, Jiandong·2016·Cold Spring Harbor Perspectives in Medicine

Abstract

P53 is a transcription factor highly inducible by many stress signals such as DNA damage, oncogene activation, and nutrient deprivation. Cell-cycle arrest and apoptosis are the most prominent outcomes of p53 activation. Many studies showed that p53 cell-cycle and apoptosis functions are important for preventing tumor development. p53 also regulates many cellular processes including metabolism, antioxidant response, and DNA repair. Emerging evidence suggests that these noncanonical p53 activities may also have potent antitumor effects within certain context. This review focuses on the cell-cycle arrest and apoptosis functions of p53, their roles in tumor suppression, and the regulation of cell fate decision after p53 activation.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1101/cshperspect.a026104

Cites

125 of 125 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage.

    “It is established that transcription factor p53 is the master regulator of the DNA damage response and is stabilized and transactivated in response to DNA damage [ 38 , 39 , 40 , 41 ].”

    From Differential Induction of Reactive Oxygen Species and Expression of Antioxidant Enzymes in Human Melanocytes Correlate with Melanin Content: Implications on the Response to Solar UV and Melanoma Susceptibility (2022) · cites this paper as [39]

    The Abstract (page unavailable) identifies p53 as a transcription factor induced by DNA damage. The Cell-Cycle Checkpoint Functions section (page unavailable) describes rapid p53 accumulation and induction of p21 after DNA double-strand breaks, supporting stabilization and transcriptional activation in that setting. It describes important checkpoint and repair functions, but does not establish the broader characterization of p53 as the master regulator of the DNA damage response. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

8 of the 133 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Chen, J.
Affiliations
Moffitt Cancer Center (US)
Corresponding author
Chen, Jiandong
Venue
Cold Spring Harbor Perspectives in Medicine
Published
2016-03
Volume
6
Issue
3
Pages
a026104
ISSN
2157-1422 (ISSN-L)
OpenAlex
W2288903023
Cited by
1,222
References
133
Citations by year
2026: 75 · 2025: 164 · 2024: 161 · 2023: 175 · 2022: 199 · 2021: 180 · 2020: 143 · 2019: 72 · 2018: 22 · 2017: 21 · 2016: 9 · 2013: 1
Type
posted content
Language
en
Open access
Locations
  • Cold Spring Harbor Perspectives in Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Florida Department of Health
  • Moffitt Cancer Center (P30CA076292, CA076292)
  • National Institutes of Health
  • National Cancer Institute (R01CA109636, CA 109636, CA076292, CA141244, R01CA141244, P30CA076292)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords
p53, cell cycle arrest, apoptosis, tumor initiation, tumor progression, tumor suppression, DNA damage response, oncogene activation, nutrient deprivation, cell fate determination, DNA repair, antioxidant response, metabolism
MeSH terms
Animals, DNA Repair, Neoplasms, Transcription Factors, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Mice, Cell Cycle Checkpoints

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