Evidence map›Paper›PMID 26806348›Full record

ArticleNeoplasia (New York, N.Y.)2016

AMOTL1 Promotes Breast Cancer Progression and Is Antagonized by Merlin.

Christophe Couderc, Alizée Boin, Laetitia Fuhrmann, Anne Vincent-Salomon, Vinay Mandati, Yann Kieffer, Fatima Mechta-Grigoriou, Laurence Del Maestro, Philippe Chavrier, David Vallerand and 7 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions ofInternational journal of molecular sciences · 2023
    Review
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  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  17. Review
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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

17 authors at 3 institutions in 1 country.

Christophe CoudercInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
Alizée BoinInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
Laetitia FuhrmannInstitut Curie, Paris, France; CNRS UMR144, Paris, France; Department of Biopathology, Paris, France.
Anne Vincent-SalomonInstitut Curie, Paris, France; Department of Biopathology, Paris, France; INSERM U934, Paris, France.
Vinay MandatiInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
Yann KiefferInstitut Curie, Paris, France; Stress and Cancer Laboratory, INSERM U830, France.
Fatima Mechta-GrigoriouInstitut Curie, Paris, France; Stress and Cancer Laboratory, INSERM U830, France.
Laurence Del MaestroInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
Philippe ChavrierInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
David VallerandInstitut Curie, Paris, France; Département de Recherche Translationnelle, Laboratoire d'Investigation Préclinique, Paris, France.
Isabelle BritoInstitut Curie, Paris, France; INSERM U900, Paris, France; Mines ParisTech, Fontainebleau, France.
Thierry DuboisInstitut Curie, Paris, France; Département de Recherche Translationnelle, Breast Cancer Biology Group, France.
Leanne De KoningInstitut Curie, Paris, France; RPPA Platform, Paris, France.
Daniel BouvardINSERM U823, Institut Albert Bonniot, Grenoble, France; Université Joseph Fourier, Grenoble, France.
Daniel LouvardInstitut Curie, Paris, France; CNRS UMR144, Paris, France.
Alexis GautreauEcole Polytechnique, CNRS UMR7654 Palaiseau, France.
Dominique LallemandInstitut Curie, Paris, France; CNRS UMR144, Paris, France. Electronic address: dominique.lallemand@inserm.fr.
Centre National de la Recherche Scientifique · FRInserm · FRInstitut Curie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Hippo signaling network is a key regulator of cell fate. In the recent years, it was shown that its implication in cancer goes well beyond the sole role of YAP transcriptional activity and its regulation by the canonical MST/LATS kinase cascade. Here we show that the motin family member AMOTL1 is an important effector of Hippo signaling in breast cancer. AMOTL1 connects Hippo signaling to tumor cell aggressiveness. We show that both canonical and noncanonical Hippo signaling modulates AMOTL1 levels. The tumor suppressor Merlin triggers AMOTL1 proteasomal degradation mediated by the NEDD family of ubiquitin ligases through direct interaction. In parallel, YAP stimulates AMOTL1 expression. The loss of Merlin expression and the induction of Yap activity that are frequently observed in breast cancers thus result in elevated AMOTL1 levels. AMOTL1 expression is sufficient to trigger tumor cell migration and stimulates proliferation by activating c-Src. In a large cohort of human breast tumors, we show that AMOTL1 protein levels are upregulated during cancer progression and that, importantly, the expression of AMOTL1 in lymph node metastasis appears predictive of the risk of relapse. Hence we uncover an important mechanism by which Hippo signaling promotes breast cancer progression by modulating the expression of AMOTL1.

Indexed as

AngiomotinsAnimalsBreast NeoplasmsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression Regulation, NeoplasticHeterograftsHumansMembrane ProteinsAMOTL1 protein, humanAngiomotinsCell Cycle ProteinsMembrane ProteinsNeurofibromin 2Nuclear Proteinssrc-Family KinasesTranscription FactorsYY1AP1 protein, human

Identifiers

PMID26806348
PMCPMC4735628
OpenAlexW2278129394

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.