Evidence map›Paper›PMID 27473335›Full record

ReviewJournal of experimental & clinical cancer research : CR2016

β-arrestin1 at the cross-road of endothelin-1 signaling in cancer.

Laura Rosanò, Anna Bagnato

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026
    Review
  3. Endogenous modulators in lung cancer.World journal of clinical cases · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. YAP and endothelin-1 signaling: an emerging alliance in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Laura RosanòPreclinical Models and New Therapeutic Agents Unit, Translational Research Functional Departmental Area, Regina Elena National Cancer Institute, Via Elio Chianesi, 53, 00144, Rome, Italy. laura.rosano@ifo.gov.it.
Anna BagnatoPreclinical Models and New Therapeutic Agents Unit, Translational Research Functional Departmental Area, Regina Elena National Cancer Institute, Via Elio Chianesi, 53, 00144, Rome, Italy. annateresa.bagnato@ifo.gov.it.
National Cancer Institute · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The advent of targeted therapeutics in human cancer has begun to find novel druggable targets and, in this context, the endothelin-1 receptor (ET-1R), namely ETA receptor (ETAR) and ETB receptor, among the GPCR family represents a class of highly druggable molecules in cancer. ET-1R are aberrantly expressed in human malignancies, potentially representing prognostic factors. Their activation by ligand stimulation initiate signaling cascades activating different downstream effectors, allowing precise control over multiple signaling pathways. ET-1R regulates cell proliferation, survival, motility, cytoskeletal changes, angiogenesis, metastasis as well as drug resistance. The molecular events underlying these responses are the activation of transcriptional factors and coactivators, and downstream genes, acting as key players in tumor growth and progression. ET-1R represent crucial cancer targets that have been exploited for ET-1R therapeutics. Importantly, efforts to explore new information of ETAR in cancer have uncovered that their functions are crucially regulated by multifunctional scaffold protein β-arrestins (β-arrs) which orchestrate the multidimensionality of ETAR signaling into highly regulated and distinct signaling complexes, a property that is highly advantageous for tumor signaling. Moreover, the role of β-arr1 in ET-1 signaling in cancer highlights why the pleiotropic effects of ET-1 and its dynamic signaling are more complex than previously recognized. In order to improve therapeutic strategies that interfere with the widespread effects of ET-1R, it is important to consider antagonists able to turn the receptors "off" selectively controlling β-arr1-dependent signaling, highlighting the possibility that targeting ETAR/β-arr1 may display a large therapeutic window in cancer.

Indexed as

beta-Arrestin 1Cell Line, TumorCell MovementCell ProliferationCell SurvivalEndothelin-1Gene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasmsReceptor, Endothelin AReceptor, Endothelin BSignal TransductionARRB1 protein, humanbeta-Arrestin 1EDNRB protein, humanEndothelin-1Receptor, Endothelin AReceptor, Endothelin BCancerEndothelinEndothelin receptorsG-protein coupled receptorsβ-arrestin

Identifiers

PMID27473335
PMCPMC4966762
OpenAlexW2498570939

What OpenQuestion holds

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LicenceCC BY
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.