Evidence map›Paper›PMID 22847613›Full record

ArticleOncogene2013

Mutant p53 gain-of-function induces epithelial-mesenchymal transition through modulation of the miR-130b-ZEB1 axis.

P Dong, M Karaayvaz, N Jia, M Kaneuchi, J Hamada, H Watari, S Sudo, J Ju, N Sakuragi

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% 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

205 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mutant p53 regulates reversible subtype plasticity in pancreatic cancer.Cellular and molecular life sciences : CMLS · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Evidence for a TMAO-HULC-miRNA regulatory axis in colorectal cancer cells.International journal of molecular and cellular medicine · 2025
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

145 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

9 authors at 4 institutions in 3 countries.

P DongDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan. dongpeix@yahoo.co.jp
M Karaayvaz
N Jia
M Kaneuchi
J Hamada
H Watari
S Sudo
J Ju
N Sakuragi
Hokkaido University · JPHokkaido University of Science · JPRuijin Hospital · CNStony Brook University · US

Funding

Molecular Mechanism of miR-140 in Colon CancerR01CA155019 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI JU, JINGFANG · 2011 to 2014
$1.5M
Identification of post-transcriptionally regulated targets by TrIP-Chip/SeqR33CA147966 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI JU, JINGFANG · 2011 to 2013
$674k
NCI NIH HHS R01 CA155019NCI NIH HHS R33 CA147966
6 · The paper itself

Abstract

The tumor suppressor gene p53 has been implicated in the regulation of epithelial-mesenchymal transition (EMT) and tumor metastasis by regulating microRNA (miRNA) expression. Here, we report that mutant p53 exerts oncogenic functions and promotes EMT in endometrial cancer (EC) by directly binding to the promoter of miR-130b (a negative regulator of ZEB1) and inhibiting its transcription. We transduced p53 mutants into p53-null EC cells, profiled the miRNA expression by miRNA microarray and identified miR-130b as a potential target of mutant p53. Ectopic expression of p53 mutants repressed the expression of miR-130b and triggered ZEB1-dependent EMT and cancer cell invasion. Loss of an endogenous p53 mutation increased the expression of miR-130b, which resulted in reduced ZEB1 expression and attenuation of the EMT phenotype. Furthermore, re-expression of miR-130b suppressed mutant p53-induced EMT and ZEB1 expression. Importantly, the expression of miR-130 was significantly reduced in EC tissues, and patients with higher expression levels of miR-130b survived longer. These data provide a novel understanding of the roles of p53 gain-of-function mutations in accelerating tumor progression and metastasis through modulation of the miR-130b-ZEB1 axis.

Indexed as

Gene Expression Regulation, NeoplasticAgedAged, 80 and overBlotting, WesternDisease ProgressionEndometrial NeoplasmsEpithelial-Mesenchymal TransitionFemaleHomeodomain ProteinsHumansMicroRNAsMiddle AgedMutationNeoplasm InvasivenessSignal TransductionTranscription FactorsHomeodomain ProteinsMicroRNAsMIRN130 microRNA, humanTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53ZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID22847613
PMCPMC3705163
OpenAlexW2080392221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.