Evidence map›Paper›PMID 23449450›Full record

ArticleCell death & disease2013

MiR203 mediates subversion of stem cell properties during mammary epithelial differentiation via repression of ΔNP63α and promotes mesenchymal-to-epithelial transition.

A J DeCastro, K A Dunphy, J Hutchinson, A L Balboni, P Cherukuri, D J Jerry, J DiRenzo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. miR-203 drives breast cancer cell differentiation.Breast cancer research : BCR · 2023
    Article
  5. Review
  6. Review
  7. Review
  8. Regulation of cancer stem cells in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. MicroRNAs in regulation of triple-negative breast cancer progression.Journal of cancer research and clinical oncology · 2018
    Review
  17. Observational
  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

7 authors at 2 institutions in 1 country.

A J DeCastroProgram in Experimental and Molecular Medicine and the Department of Pharmacology, The Geisel School of Medicine at Dartmouth, Hanover, NH, USA.
K A Dunphy
J Hutchinson
A L Balboni
P Cherukuri
D J Jerry
J DiRenzo
Dartmouth College · USUniversity of Massachusetts Amherst · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Fred W Kolling IV · 1985 to 2026
$91.3M
Role of DN-p63 in Preservation of Self RenewalR01CA108539 · NCI · DARTMOUTH COLLEGE · PI DIRENZO, JAMES · 2005 to 2009
$1.4M
NCI NIH HHS 5R01CA108539NCI NIH HHS P30 CA023108NCI NIH HHS R01 CA108539
6 · The paper itself

Abstract

During reproductive life, the mammary epithelium undergoes consecutive cycles of proliferation, differentiation and apoptosis. Doing so relies on the retained proliferative capacity, prolonged lifespan and developmental potency of mammary stem cells (MaSCs). ΔNp63α, the predominant TP63 isoform in mammary epithelia, is robustly expressed in MaSCs and is required for preservation of self-renewing capacity in diverse epithelial structures. However, the mechanism(s) underlying subversion of this activity during forfeiture of self-renewing capacity are poorly understood. MicroRNAs (miRNAs) govern critical cellular functions including stem cell maintenance, development, cell cycle regulation and differentiation by disrupting translation of target mRNAs. Data presented here indicate that expression of miR203, a miRNA that targets ΔNp63α and ΔNp63β is activated during luminal epithelial differentiation and that this pattern is observed in the murine mammary hierarchy. In addition, we present evidence that the transcription factor Zeb1 represses miR203 expression, thus enhancing ΔNp63α protein levels. Furthermore, ectopic miR203 suppresses ΔNp63α expression, proliferation and colony formation. The anti-clonogenic effects mediated by miR203 require suppression of ΔNp63α. In addition, ectopic miR203 promotes mesenchymal-to-epithelial transition and disrupts activities associated with epithelial stem cells. These studies support a model in which induction of miR203 mediates forfeiture of self-renewing capacity via suppression of ΔNp63α and may also have anti-tumorigenic activity through its reduction of EMT and cancer stem cell populations.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell DifferentiationCell LineG1 Phase Cell Cycle CheckpointsHomeodomain ProteinsHumansMammary Glands, AnimalMammary Glands, HumanMCF-7 CellsMiceMicroRNAsNeoplastic Stem CellsProtein IsoformsRNA InterferenceRNA, Small InterferingHomeodomain ProteinsMicroRNAsMIRN203 microRNA, humanProtein IsoformsRNA, Small InterferingTP63 protein, humanTranscription FactorsTumor Suppressor ProteinsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID23449450
PMCPMC3734833
OpenAlexW2096609001

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.