Evidence map›Paper›PMID 29855541›Full record

ArticleCell death and differentiation2019

The Ectodysplasin receptor EDAR acts as a tumor suppressor in melanoma by conditionally inducing cell death.

Jonathan Vial, Amélie Royet, Philippe Cassier, Antonin Tortereau, Sarah Dinvaut, Denis Maillet, Lise Gratadou-Hupon, Marion Creveaux, Alexa Sadier, Garance Tondeur and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  7. Ectodysplasin A (EDA) Signaling: From Skin Appendage to Multiple Diseases.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Embryonic Programs in Cancer and Metastasis-Insights From the Mammary Gland.Frontiers in cell and developmental biology · 2022
    Review
  10. Review
  11. Article
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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

19 authors at 5 institutions in 1 country.

Jonathan VialDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Amélie RoyetDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Philippe CassierDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Antonin TortereauNational Veterinary School, F-69280 Marcy L'Etoile, Lyon, France.
Sarah DinvautDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Denis MailletDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Lise Gratadou-HuponDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Marion CreveauxDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France.
Alexa SadierUnivLyon, ENS de Lyon, Université de Lyon, CNRS UMR5239, INSERM U1210, Lyon, France.
Garance TondeurDepartment of Dermatology, Centre Hospitalier Lyon Sud, Pierre Bénite, France.
Sophie LéonAnatomopathology service, Centre Léon Bérard, 69008, Lyon, France.
Lauriane DepaepeDepartment of Dermatology, Centre Hospitalier Lyon Sud, Pierre Bénite, France.
Sophie PantalacciUnivLyon, ENS de Lyon, Université de Lyon, CNRS UMR5239, INSERM U1210, Lyon, France.
Arnaud de la FouchardièreAnatomopathology service, Centre Léon Bérard, 69008, Lyon, France.
Olivier MicheauInstitut National de la Santé et de la Recherche Médicale, UMR866, F-21079, Dijon, France.ORCID http://orcid.org/0000-0001-8499-7984
Stéphane DalleDepartment of Dermatology, Centre Hospitalier Lyon Sud, Pierre Bénite, France.
Vincent LaudetObservatoire Océanologique de Banyuls-sur-Mer, 1, avenue du Fontaulé, 66650, Banyuls-sur-Mer, France.
Patrick MehlenDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France. patrick.mehlen@lyon.unicancer.fr.
Marie CastetsDependence Receptors, Cancer and Development Laboratory - Equipe labellisée 'La Ligue', LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008, Lyon, France. marie.castets@lyon.unicancer.fr.
Université Claude Bernard Lyon 1 · FRHôpital Lyon Sud · FRCentre Léon Bérard · FRInserm · FRObservatoire Océanologique de Banyuls-sur-Mer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ectodysplasin receptor EDAR is seen as a typical Tumor Necrosis Factor receptor (TNFR) family member known to interact with its ligand Eda-A1, and signaling mainly through the nuclear factor-kappaB (NF-κB) and c-jun N-terminal kinases pathways. Mutations in genes that encode proteins involved in EDAR transduction cascade cause anhidrotic ectodermal dysplasia. Here, we report an unexpected pro-apoptotic activity of EDAR when unbound to its ligand Eda-A1, which is independent of NF-κB pathway. Contrarily to other death receptors, EDAR does recruit caspase-8 to trigger apoptosis but solely upon ligand withdrawal, thereby behaving as the so-called dependence receptors. We propose that pro-apoptotic activity of unbound EDAR confers it a tumor suppressive activity. Along this line, we identified loss-of-pro-apoptotic function mutations in EDAR gene in human melanoma. Moreover, we show that the invalidation of EDAR in mice promotes melanoma progression in a B-Raf mutant background. Together, these data support the view that EDAR constrains melanoma progression by acting as a dependence receptor.

Indexed as

AnimalsCell DeathCell Line, TumorEctodysplasinsEdar ReceptorFemaleHEK293 CellsHumansMelanomaMiceMice, Inbred C57BLMice, KnockoutMice, NudeMutationEctodysplasinsEDA protein, humanEDAR protein, humanEdar protein, mouseEdar Receptor

Identifiers

PMID29855541
PMCPMC6370843
OpenAlexW2807011331

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.