Evidence map›Paper›PMID 22894933›Full record

ArticleCell cycle (Georgetown, Tex.)2012

p53 negatively regulates Aurora A via both transcriptional and posttranslational regulation.

Chun-Chi Wu, Tsung-Ying Yang, Chang-Tze Ricky Yu, Liem Phan, Cristina Ivan, Anil K Sood, Shih-Lan Hsu, Mong-Hong Lee

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. TF-DUBTACs Stabilize Tumor Suppressor Transcription Factors.Journal of the American Chemical Society · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Chun-Chi WuInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan, Republic of China.
Tsung-Ying Yang
Chang-Tze Ricky Yu
Liem Phan
Cristina Ivan
Anil K Sood
Shih-Lan Hsu
Mong-Hong Lee
The University of Texas MD Anderson Cancer Center · USTaichung Veterans General Hospital · TWChung Shan Medical University Hospital · TWNational Chi Nan University · TW

Funding

Regulation of cyclin-dependent kinase inhibitor p27 in cancerR01CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2002 to 2013
$2.8M
NCI NIH HHS R01 CA089266NCI NIH HHS R01CA089266
6 · The paper itself

Abstract

p53 plays an important role in mitotic checkpoint, but what its role is remains enigmatic. Aurora A is a Ser/Thr kinase involved in correcting progression of mitosis. Here, we show that p53 is a negative regulator for Aurora A. We found that p53 deficiency leads to Aurora A elevation. Ectopic expression of p53 or DNA damage-induced expression of p53 can suppress the expression of Aurora A. Mechanistic studies show that p53 is a negative regulator for Aurora A expression through both transcriptional and posttranslational regulation. p53 knockdown in cancer cells reduces the level of p21, which, in turn, increases the activity of CDK2 followed by induction of Rb1 hyperphosphorylation and its dissociation with transcriptional factor E2F3. E2F3 can bind to Aurora A gene promoter, potentiating Aurora A gene expression and p53 deficiency, enhancing the binding of E2F3 on Aurora A promoter. Also, p53 deficiency leads to decelerating Aurora A's turnover rate, due to the fact that p53 deficiency causes the downregulation of Fbw7α, a component of E3 ligase of Aurora A. Consistently, p53 knockdown-mediated Aurora A elevation is mitigated when Fbw7α is ectopically expressed. Thus, p53-mediated Aurora A degradation requires Fbw7α expression. Significantly, inverse correlation between p53 and Aurora A elevation is translated into the deregulation of centrosome amplification. p53 knockdown leads to high percentages of cells with abnormal amplification of centrosome. These data suggest that p53 is an important negative regulator of Aurora A, and that loss of p53 in many types of cancer could lead to abnormal elevation of Aurora A and dysregulated mitosis, which provides a growth advantage for cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAurora KinasesCentrosomeCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesDown-RegulationE2F3 Transcription FactorFemaleGene Knockdown TechniquesHumansModels, BiologicalOvarian NeoplasmsPromoter Regions, GeneticProtein BindingProtein BiosynthesisAurora KinasesCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesE2F3 Transcription FactorProtein Serine-Threonine KinasesRetinoblastoma ProteinRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID22894933
PMCPMC3466554
OpenAlexW2068678285

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.