Evidence map›Paper›PMID 23208497›Full record

ArticleOncogene2013

β-arrestin-1 is a nuclear transcriptional regulator of endothelin-1-induced β-catenin signaling.

L Rosanò, R Cianfrocca, P Tocci, F Spinella, V Di Castro, F Spadaro, E Salvati, A M Biroccio, P G Natali, A Bagnato

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
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

54 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. New Target(s) for RNF43 Regulation: Implications for Therapeutic Strategies.International journal of molecular sciences · 2024
    Review
  6. Endothelin and the tumor microenvironment: a finger in every pie.Clinical science (London, England : 1979) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Biochemical and physiological insights into TRH receptor-mediated signaling.Frontiers in cell and developmental biology · 2022
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. YAP and endothelin-1 signaling: an emerging alliance in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  17. Article
  18. Article
  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

10 authors at 1 institution in 1 country.

L RosanòLaboratory of Molecular Pathology, Regina Elena National Cancer Institute, Rome, Italy.
R Cianfrocca
P Tocci
F Spinella
V Di Castro
F Spadaro
E Salvati
A M Biroccio
P G Natali
A Bagnato
Istituto Superiore di Sanità · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the fundamental pathophysiological importance of β-catenin in tumor progression, the mechanism underlying its final transcriptional output has been partially elucidated. Here, we report that β-arrestin-1 (β-arr1) is an epigenetic regulator of endothelin (ET)-1-induced β-catenin signaling in epithelial ovarian cancer (EOC). In response to ET A receptor (ETAR) activation by ET-1, β-arr1 increases its nuclear translocation and direct binding to β-catenin. This in turn enhanced β-catenin nuclear accumulation and transcriptional activity, which was prevented by expressing a mutant β-arr1 incapable of nuclear distribution. β-arr1-β-catenin interaction controls β-catenin target gene expressions, such as ET-1, Axin 2, Matrix metalloproteinase 2, and Cyclin D1, by promoting histone deacetylase 1 (HDAC1) dissociation and the recruitment of p300 acetyltransferase on these promoter genes, resulting in enhanced H3 and H4 histone acetylation, and gene transcription, required for cell migration, invasion and epithelial-to-mesenchymal transition. These effects are abrogated by β-arr1 silencing or by mutant β-arr1, as well as by β-catenin or p300 silencing, confirming that nuclear β-arr1 forms a functional complex capable of regulating epigenetic changes in β-catenin-driven invasive behavior. In a murine orthotopic model of metastatic human EOC, silencing of β-arr1 or mutant β-arr1 expression, as well as ETAR blockade, inhibits metastasis. In human EOC tissues, β-arr1-β-catenin nuclear complexes are selectively enriched at β-catenin target gene promoters, correlating with tumor grade, confirming a direct in vivo β-arr1-β-catenin association at specific set of genes involved in EOC progression. Collectively, our study provides insights into how a β-arr1-mediated epigenetic mechanism controls β-catenin activity, unraveling new components required for its nuclear function in promoting metastasis.

Indexed as

AnimalsArrestinsAxin Proteinbeta-Arrestin 1beta-Arrestinsbeta CateninCarcinoma, Ovarian EpithelialCell NucleusCyclin D1Endothelin-1Epigenesis, GeneticEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone Deacetylase 1HistonesARRB1 protein, humanArrb1 protein, mouseArrestinsAXIN2 protein, humanAxin Proteinbeta-Arrestin 1beta-Arrestinsbeta CateninCCND1 protein, humanCyclin D1Endothelin-1HDAC1 protein, humanHistone Deacetylase 1HistonesMatrix Metalloproteinase 2Receptor, Endothelin A

Identifiers

PMID23208497
OpenAlexW2012628363

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.