Evidence map›Paper›PMID 25111861›Full record

ArticleOncogenesis2014

The Yes-associated protein controls the cell density regulation of Hedgehog signaling.

M Tariki, P K Dhanyamraju, V Fendrich, T Borggrefe, G Feldmann, M Lauth

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Hippo/YAP signaling's multifaceted crosstalk in cancer.Frontiers in cell and developmental biology · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Implications of Cellular Mechanical Memory in Bioengineering.ACS biomaterials science & engineering · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. WNT signaling and cancer stemness.Essays in biochemistry · 2022
    Article
  11. Cancers · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. DYRK1B regulates Hedgehog-induced microtubule acetylation.Cellular and molecular life sciences : CMLS · 2019
    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

6 authors at 4 institutions in 1 country.

M TarikiInstitute of Molecular Biology and Tumor Research (IMT), Center for Tumor and Immunobiology, Philipps University, Marburg, Germany.
P K DhanyamrajuInstitute of Molecular Biology and Tumor Research (IMT), Center for Tumor and Immunobiology, Philipps University, Marburg, Germany.
V FendrichDepartment of Surgery, Philipps University, Marburg, Germany.
T BorggrefeInstitute of Biochemistry, Justus-Liebig University, Giessen, Germany.
G FeldmannCenter of Integrated Oncology Cologne-Bonn, University of Bonn, Bonn, Germany.
M LauthInstitute of Molecular Biology and Tumor Research (IMT), Center for Tumor and Immunobiology, Philipps University, Marburg, Germany.
Institute of Molecular Biology · DEPhilipps University of Marburg · DEUniversity of Bonn · DEUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evolutionarily conserved Hedgehog (Hh) signaling pathway is essential for correct embryogenesis and is misregulated in several malignancies. In cell culture, Hh-sensitive cells display a striking dependence on cell density with active Hh signaling requiring cell-to-cell contact. As the Hippo/YAP system is tightly linked to cell density control and contact inhibition, we investigated the cross-talk between the two pathways. Our data reveal that the suppression of Hh signaling in the absence of cellular contacts is independent of primary cilia and is mediated by the YAP oncogene. Overexpression of YAP blocks Hh signaling whereas RNA interference-mediated knockdown of YAP enhances Hh/GLI activity. Despite this negative regulation, Hh signaling promotes YAP activity through post-transcriptional mechanisms, resulting in a negative feedback loop. In vivo, we found strong nuclear YAP immunoreactivity restricted to compartments with low Hh pathway activity in human and mouse pancreatic cancer. Finally, we identified protease-activated receptors (PARs) as molecules being able to override the inverse Hippo/Hh regulation, potentially giving tumors a mechanism to utilize both oncogenic pathways in parallel.Oncogenesis (2014) 3, e112; doi:10.1038/oncsis.2014.27; published online 11 August 2014.

Identifiers

PMID25111861
PMCPMC5189961
OpenAlexW2009129074

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.