Evidence map›Paper›PMID 19549682›Full record

ArticleJournal of cell science2009

Regulation of beta 4-integrin expression by epigenetic modifications in the mammary gland and during the epithelial-to-mesenchymal transition.

Xiaofang Yang, Bryan Pursell, Shaolei Lu, Tsun-Kai Chang, Arthur M Mercurio

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024
    Review
  3. Article
  4. Epigenetic regulation and targeting of ECM for cancer therapy.American journal of physiology. Cell physiology · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Integrins and Cell Metabolism: An Intimate Relationship Impacting Cancer.International journal of molecular sciences · 2017
    Review
  19. 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

5 authors at 1 institution in 1 country.

Xiaofang YangDepartment of Cancer Biology and Cancer Center, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Bryan Pursell
Shaolei Lu
Tsun-Kai Chang
Arthur M Mercurio
University of Massachusetts Chan Medical School · US

Funding

INTEGRIN FUNCTION AND SIGNALING IN CARCINOMA PROGRESSIONR01CA080789 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MERCURIO, ARTHUR M · 1999 to 2012
$4.7M
NCI NIH HHS CA1107548NCI NIH HHS CA80789NCI NIH HHS R01 CA080789PHS HHS T32130807
6 · The paper itself

Abstract

The beta 4 integrin is expressed in epithelial cells, a few other cell types and in some carcinomas. Despite this restricted expression pattern and the functional importance of beta 4 integrin in epithelial and carcinoma biology, little is known about how its expression is regulated. Here, we assessed the epigenetic regulation of beta 4 integrin based on the presence of a large CpG island in the beta 4-integrin gene promoter. We separated basal (beta 4+) and luminal (beta 4-) epithelial cells from the mammary glands of K14-eGFP mice and demonstrated that the beta 4-integrin promoter is unmethylated in basal cells and methylated in luminal cells. We also observed that expression of beta 4 integrin and E-cadherin is lost during the epithelial-to-mesenchymal transition (EMT) of mammary gland cells induced by transforming growth factor beta (TGFbeta), which is coincident with de novo DNA methylation, a decrease in active histone modifications (H3K9Ac and H3K4me3) and an increase in the repressive histone modification H3K27me3. Furthermore, TGFbeta withdrawal promotes a mesenchymal-to-epithelial transition (MET) and triggers the re-expression of beta 4 integrin and E-cadherin. Intriguingly, demethylation at either promoter is not obligatory for transcriptional reactivation after TGFbeta withdrawal. However, both H3K9Ac and H3K4me3 modifications are restored during the MET, and H3K27me3 is reduced, strongly suggesting that reversible histone modifications rather than DNA demethylation are the predominant factors in reactivating expression of these genes. Our data indicate that complex epigenetic modifications contribute to the regulation of the beta 4 integrin and E-cadherin.

Indexed as

DNA MethylationAnimalsCadherinsCell LineCell TransdifferentiationCpG IslandsEpithelial CellsFemaleHistonesIntegrin beta4Mammary Glands, AnimalMesodermMiceMice, TransgenicPromoter Regions, GeneticTranscriptional ActivationCadherinsHistonesIntegrin beta4Transforming Growth Factor beta

Identifiers

PMID19549682
PMCPMC2704882
OpenAlexW2159186384

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.