Evidence map›Paper›PMID 24374014›Full record

ReviewCancer letters2015

Tumor suppressor p53 and its mutants in cancer metabolism.

Juan Liu, Cen Zhang, Wenwei Hu, Zhaohui Feng

Abstract readReview
In one paragraph

Review in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

148 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
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  8. Review
  9. Article
  10. Article
  11. Article
  12. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  13. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  14. Review
  15. Interplay between altered metabolism and DNA damage and repair in ovarian cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  16. Cells · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Review

88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Juan LiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ 08903, USA.
Cen ZhangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ 08903, USA.
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ 08903, USA; Department of Pediatrics, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ 08903, USA.
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ 08903, USA. Electronic address: fengzh@cinj.rutgers.edu.

Funding

The Role of LIF, a Novel Negative Regulator of p53, in Colorectal CancerR01CA160558 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HU, WENWEI · 2012 to 2017
$1.6M
The role of glutaminase 2, a novel p53 target gene in metabolism, in liver cancerR01CA143204 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI FENG, ZHAOHUI · 2010 to 2014
$1.6M
NCI NIH HHS R01 CA143204NCI NIH HHS R01CA143204NCI NIH HHS R01 CA160558NCI NIH HHS R01CA160558
6 · The paper itself

Abstract

Tumor-suppressor p53 plays a key role in tumor prevention. As a transcription factor, p53 transcriptionally regulates its target genes to initiate different biological processes in response to stress, including apoptosis, cell cycle arrest or senescence, to exert its function in tumor suppression. Recent studies have revealed that metabolic regulation is a novel function of p53. Metabolic changes have been regarded as a hallmark of tumors and a key contributor to tumor development. p53 regulates many different aspects of metabolism, including glycolysis, mitochondrial oxidative phosphorylation, pentose phosphate pathway, fatty acid synthesis and oxidation, to maintain the homeostasis of cellular metabolism, which contributes to the role of p53 in tumor suppression. p53 is frequently mutated in human tumors. In addition to loss of tumor suppressive function, tumor-associated mutant p53 proteins often gain new tumorigenic activities, termed gain-of-function of mutant p53. Recent studies have shown that mutant p53 mediates metabolic changes in tumors as a novel gain-of-function to promote tumor development. Here we review the functions and mechanisms of wild-type and mutant p53 in metabolic regulation, and discuss their potential roles in tumorigenesis.

Indexed as

ApoptosisCell Cycle CheckpointsCell Transformation, NeoplasticCellular SenescenceEnergy MetabolismFatty AcidsGlycolysisHumansMitochondriaMutationNeoplasmsOxidative PhosphorylationPentose Phosphate PathwaySignal TransductionTumor Suppressor Protein p53Fatty AcidsTumor Suppressor Protein p53MetabolismMutant p53p53Tumor suppressor

Identifiers

PMID24374014
PMCPMC4069248

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.