Evidence map›Paper›PMID 22024162›Full record

ArticleThe Journal of cell biology2011

A p53/miRNA-34 axis regulates Snail1-dependent cancer cell epithelial-mesenchymal transition.

Nam Hee Kim, Hyun Sil Kim, Xiao-Yan Li, Inhan Lee, Hyung-Seok Choi, Shi Eun Kang, So Young Cha, Joo Kyung Ryu, Dojun Yoon, Eric R Fearon and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 261 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
261citing papers in PubMed, 1 pooled it
19.6field-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

261 citing papers in PubMed, 1 synthesis or guideline pooled it, 435 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  13. Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. How MicroRNAs Command the Battle against Cancer.International journal of molecular sciences · 2024
    Review
  20. Review

201 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

15 authors at 6 institutions in 3 countries.

Nam Hee KimDepartment of Oral Pathology, Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul 120-752, South Korea.
Hyun Sil Kim
Xiao-Yan Li
Inhan Lee
Hyung-Seok Choi
Shi Eun Kang
So Young Cha
Joo Kyung Ryu
Dojun Yoon
Eric R Fearon
R Grant Rowe
Sanghyuk Lee
Christopher A Maher
Stephen J Weiss
Jong In Yook
Yonsei University · KRInstitute of Human Genetics · PLEwha Womans University · KRCatholic Kwandong University · KRMichigan Center for Translational Pathology · USUniversity of Michigan–Ann Arbor · US

Funding

SNAIL-Dependent Regulation of EMT in CancerR01CA116516 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WEISS, STEPHEN J · 2006 to 2010
$1.2M
NCI NIH HHS 5R01CA116516-5NCI NIH HHS R01 CA116516
6 · The paper itself

Abstract

Snail1 is a zinc finger transcriptional repressor whose pathological expression has been linked to cancer cell epithelial-mesenchymal transition (EMT) programs and the induction of tissue-invasive activity, but pro-oncogenic events capable of regulating Snail1 activity remain largely uncharacterized. Herein, we demonstrate that p53 loss-of-function or mutation promotes cancer cell EMT by de-repressing Snail1 protein expression and activity. In the absence of wild-type p53 function, Snail1-dependent EMT is activated in colon, breast, and lung carcinoma cells as a consequence of a decrease in miRNA-34 levels, which suppress Snail1 activity by binding to highly conserved 3' untranslated regions in Snail1 itself as well as those of key Snail1 regulatory molecules, including β-catenin, LEF1, and Axin2. Although p53 activity can impact cell cycle regulation, apoptosis, and DNA repair pathways, the EMT and invasion programs initiated by p53 loss of function or mutation are completely dependent on Snail1 expression. These results identify a new link between p53, miR-34, and Snail1 in the regulation of cancer cell EMT programs.

Indexed as

Apoptosisbeta CateninEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHCT116 CellsHumansLymphoid Enhancer-Binding Factor 1MicroRNAsMicroscopy, ConfocalNeoplasm InvasivenessNeoplasmsSnail Family Transcription FactorsTranscription FactorsTumor Cells, CulturedTumor Suppressor Protein p53beta CateninLEF1 protein, humanLymphoid Enhancer-Binding Factor 1MicroRNAsMIRN34 microRNA, humanSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID22024162
PMCPMC3206336
OpenAlexW2155487079

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.