Evidence map›Paper›PMID 22457351›Full record

ArticleThe Journal of biological chemistry2012

Mammary epithelial cell polarity is regulated differentially by p73 isoforms via epithelial-to-mesenchymal transition.

Yanhong Zhang, Wensheng Yan, Yong Sam Jung, Xinbin Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Frontiers in cell and developmental biology · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021
    Review
  7. Cancer Stemness: p53 at the Wheel.Frontiers in oncology · 2020
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Therapeutic targeting of the p53 pathway in cancer stem cells.Expert opinion on therapeutic targets · 2012
    Review
  20. Article
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 at 1 institution in 1 country.

Yanhong ZhangComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Wensheng YanComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Yong Sam JungComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Xinbin ChenComparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616. Electronic address: xbchen@ucdavis.edu.
University of California, Davis · US

Funding

MECHANISM OF P73 DEPENDENT TUMOR SUPPRESSIONR01CA081237 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 1999 to 2022
$6.8M
NCI NIH HHS CA081237NCI NIH HHS R01 CA081237
6 · The paper itself

Abstract

p73 is expressed as TA and ΔN isoforms, both of which are implicated in tumor suppression and/or promotion. To address how p73 possesses these opposing functions, we developed three-dimensional culture of MCF10A cells, which undergo cell morphogenesis to form polarized spheroids with hollow lumen similar to normal mammary acini in vivo. Here, we showed that upon knockdown of p73, particularly TAp73 but not ΔNp73, MCF10A cells formed irregular and near-normal acini without hollow lumen in three-dimensional culture. We also found that upon knockdown of p73 or TAp73, but not ΔNp73, MCF10A cells underwent epithelial-to-mesenchymal transition (EMT) via down-regulation of E-cadherin coupled with up-regulation of β-catenin and laminin V. In addition, we found that Snail-1, Slug, and Twist, all of which are known to act as EMT inducers by repressing E-cadherin expression, were increased markedly upon knockdown of p73 and TAp73 but little if any by ΔNp73. Furthermore, we showed that knockdown of p73 or TAp73 in MCF10A cells led to a marked increase in cell proliferation and migration. Together, our data suggest that TAp73 is necessary for maintaining normal cell polarity by suppressing EMT.

Indexed as

beta CateninCadherinsCell Adhesion MoleculesCell Line, TransformedCell PolarityCell ProliferationDNA-Binding ProteinsDown-RegulationEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHumansKalininMammary Glands, HumanNuclear Proteinsbeta CateninCadherinsCell Adhesion Moleculesdelta Np73 protein, humanDNA-Binding ProteinsKalininNuclear ProteinsSNAI1 protein, humanSnail Family Transcription FactorsTP73 protein, humanTranscription FactorsTumor Protein p73Tumor Suppressor ProteinsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID22457351
PMCPMC3366836
OpenAlexW2040318436

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.