Evidence map›Paper›PMID 23542170›Full record

ArticleOncogene2014

P63 regulates tubular formation via epithelial-to-mesenchymal transition.

Y Zhang, W Yan, X Chen

Abstract read
In one paragraph

Article in Oncogene, 2014. 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
1.3field-weighted citation impact, top 20% 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, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The dual role of p63 in cancer.Frontiers in oncology · 2023
    Review
  6. The DeltaN p63 Promotes EMT and Metastasis in Bladder Cancer by the PTEN/AKT Signalling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. ΔNp63γ/SRC/Slug Signaling Axis Promotes Epithelial-to-Mesenchymal Transition in Squamous Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. ΔNp63α is a common inhibitory target in oncogenic PI3K/Ras/Her2-induced cell motility and tumor metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Y ZhangCenter for Comparative Oncology, Schools of Medicine and Veterinary Medicine, University of California at Davis, Davis, CA, USA.
W YanCenter for Comparative Oncology, Schools of Medicine and Veterinary Medicine, University of California at Davis, Davis, CA, USA.
X ChenCenter for Comparative Oncology, Schools of Medicine and Veterinary Medicine, University of California at Davis, Davis, CA, USA.
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
Mechanism of p53-Mediated Tumor SuppressionR01CA076069 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2002 to 2017
$4.5M
The transcriptional activity of p63, a p53 family memberR01CA102188 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2003 to 2012
$2.9M
The role of DNA polymerase eta in DNA damage response and p53 activationR01CA123227 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2010 to 2014
$1.4M
MECHANISM OF P53 DEPENDENT APOPTOSISR29CA076069 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, XINBIN · 1998 to 2002
$276k
NCI NIH HHS CA076069NCI NIH HHS CA102188NCI NIH HHS CA108122NCI NIH HHS R01 CA076069NCI NIH HHS R01 CA081237NCI NIH HHS R01 CA102188NCI NIH HHS R01 CA123227NCI NIH HHS R29 CA076069
6 · The paper itself

Abstract

P63, a p53 family member, is expressed as TA and ΔN isoforms. Interestingly, both TAp63 and ΔNp63 are transcription factors, and regulate both common and distinct sets of target genes. p63 is required for survival of some epithelial cell lineages, and lack of p63 leads to loss of epidermis and other epithelia in humans and mice. Here, we explored the role of p63 isoforms in cell proliferation, migration and tubulogenesis by using Madin-Darby Canine Kidney (MDCK) tubular epithelial cells in two- or three-dimensional (2-D or 3-D) culture. We found that like downregulation of p53, downregulation of p63 and TAp63 decreases expression of growth-suppressing genes, including p21, PUMA and MIC-1, and consequently promotes cell proliferation and migration in 2-D culture. However, in 3-D culture, downregulation of p63, especially TAp63, but not p53, decapacitates MDCK cells to form a cyst structure through enhanced epithelial-to-mesenchymal transition (EMT). In contrast, downregulation of ΔNp63 inhibits MDCK cell proliferation and migration in 2-D culture, and delays but does not block MDCK cell cyst formation and tubulogenesis in 3-D culture. Consistent with this, downregulation of ΔNp63 markedly upregulates growth-suppressing genes, including p21, PUMA and MIC-1. Taken together, these data suggest that TAp63 is the major isoform required for tubulogenesis by maintaining an appropriate level of EMT, whereas ΔNp63 fine-tunes the rate of cyst formation and tubulogenesis by maintaining an appropriate expression level of genes involved in cell cycle arrest and apoptosis.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell MovementCell ProliferationDogsEpithelial CellsGene Knockdown TechniquesMadin Darby Canine Kidney CellsProtein IsoformsTumor Suppressor ProteinsUp-RegulationProtein IsoformsTumor Suppressor Proteins

Identifiers

PMID23542170
PMCPMC4905556
OpenAlexW2091269753

What OpenQuestion holds

Textmetadata
LicenceTDM
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.