Evidence map›Paper›PMID 22618028›Full record

ArticleMolecular cancer research : MCR2012

Yes-associated protein 1 is activated and functions as an oncogene in meningiomas.

Gilson S Baia, Otavia L Caballero, Brent A Orr, Anita Lal, Janelle S Y Ho, Cynthia Cowdrey, Tarik Tihan, Christian Mawrin, Gregory J Riggins

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Malignant Meningiomas: From Diagnostics to Treatment.Diagnostics (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Preclinical Models of Meningioma.Advances in experimental medicine and biology · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Molecular neuropathology of brain-invasive meningiomas.Brain pathology (Zurich, Switzerland) · 2022
    Review
  19. Review
  20. Review
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

9 authors at 1 institution in 1 country.

Gilson S BaiaLudwig Collaborative Laboratory, Neurosurgery Department, The Johns Hopkins University, Baltimore, MD 21231, USA. gbaia1@jhmi.edu
Otavia L Caballero
Brent A Orr
Anita Lal
Janelle S Y Ho
Cynthia Cowdrey
Tarik Tihan
Christian Mawrin
Gregory J Riggins
Otto-von-Guericke University Magdeburg · DE

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

The Hippo signaling pathway is functionally conserved in Drosophila melanogaster and mammals, and its proposed function is to control tissue homeostasis by regulating cell proliferation and apoptosis. The core components are composed of a kinase cascade that culminates with the phosphorylation and inhibition of Yes-associated protein 1 (YAP1). Phospho-YAP1 is retained in the cytoplasm. In the absence of Hippo signaling, YAP1 translocates to the nucleus, associates with co-activators TEAD1-4, and functions as a transcriptional factor promoting the expression of key target genes. Components of the Hippo pathway are mutated in human cancers, and deregulation of this pathway plays a role in tumorigenesis. Loss of the NF2 tumor suppressor gene is the most common genetic alteration in meningiomas, and the NF2 gene product, Merlin, acts upstream of the Hippo pathway. Here, we show that primary meningioma tumors have high nuclear expression of YAP1. In meningioma cells, Merlin expression is associated with phosphorylation of YAP1. Using an siRNA transient knockdown of YAP1 in NF2-mutant meningioma cells, we show that suppression of YAP1 impaired cell proliferation and migration. Conversely, YAP1 overexpression led to a strong augment of cell proliferation and anchorage-independent growth and restriction of cisplatin-induced apoptosis. In addition, expression of YAP1 in nontransformed arachnoidal cells led to the development of tumors in nude mice. Together, these findings suggest that in meningiomas, deregulation of the Hippo pathway is largely observed in primary tumors and that YAP1 functions as an oncogene promoting meningioma tumorigenesis.

Indexed as

Adaptor Proteins, Signal TransducingBrain NeoplasmsMeningiomaPhosphoproteinsAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationCisplatinGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceNeoplasms, ExperimentalRNA, Small InterferingAdaptor Proteins, Signal TransducingCisplatinPhosphoproteinsRNA, Small InterferingTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID22618028
PMCPMC4703097
OpenAlexW2156989949

What OpenQuestion holds

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Registered trials

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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.