Evidence map›Paper›PMID 28069666›Full record

ReviewJournal of molecular cell biology2017

Negative auto-regulators trap p53 in their web.

Xiang Zhou, Bo Cao, Hua Lu

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 9% of its field
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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. A molecular mechanism for the "digital" response of p53 to stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023
    Review
  4. Context-Dependent Function of Long Noncoding RNAMolecular and cellular biology · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Mutant p53 in cancer therapy-the barrier or the path.Journal of molecular cell biology · 2019
    Review
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

3 authors at 2 institutions in 2 countries.

Xiang ZhouFudan University Shanghai Cancer Center and the Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Bo CaoDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Hua LuDepartment of Biochemistry & Molecular Biology and Tulane Cancer Center, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Tulane University · USFudan University Shanghai Cancer Center · CN

Funding

The Role of Ribosomal Proteins in the P53-MDM2 PathwayR01CA095441 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2002 to 2021
$5.1M
Role of the AMPK-MDMX-p53 pathway in cancerR01CA127724 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2007 to 2019
$3.0M
Dual Targeting of the p53 pathway for development of anti-cancer therapyR01CA172468 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2012 to 2016
$1.5M
Role of TFIIS.h in regulation of p53 responsive apoptosis and tumor suppressionR21CA201889 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LU, HUA · 2016 to 2017
$360k
NCI NIH HHS R01 CA095441NCI NIH HHS R01 CA127724NCI NIH HHS R01 CA172468NCI NIH HHS R21 CA201889
6 · The paper itself

Abstract

The transcriptional factor p53 activates the expression of a myriad of target genes involving a complicated signalling network, resulting in various cellular outcomes, such as growth arrest, senescence, apoptosis, and metabolic changes, and leading to consequent suppression of tumour growth and progression. Because of the profoundly adverse effect of p53 on growth and proliferation of cancer cells, several feedback mechanisms have been employed by the cells to constrain p53 activity. Two major antagonists MDM2 and MDMX (the long forms) are transcriptionally induced by p53, but in return block p53 activity, forming a negative feedback circuit and rendering chemoresistance of several cancer cells. However, they are not alone, as cancer cells also employ other proteins encoded by p53 target genes to inhibit p53 activity at transcriptional, translational, and posttranslational levels. This essay is thus composed to review a recent progress in understanding the mechanisms for how cancer cells hijack the p53 autoregulation by these proteins for their growth advantage and to discuss the clinical implications of these autoregulatory loops.

Indexed as

AnimalsDrug Resistance, NeoplasmHumansModels, BiologicalProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Proto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53chemoresistancefeedback loopMDM2NGFRp53transcription

Identifiers

PMID28069666
PMCPMC5907828
OpenAlexW2569552567

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.