Evidence map›Paper›PMID 34293352›Full record

ArticleThe Journal of investigative dermatology2022

Oncogenic Hedgehog-Smoothened Signaling Depends on YAP1‒TAZ/TEAD Transcription to Restrain Differentiation in Basal Cell Carcinoma.

Yao Yuan, Natalia Salinas Parra, Qianming Chen, Ramiro Iglesias-Bartolome

Open access · hybridAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2022. 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
1.5field-weighted citation impact, top 19% 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, 23 citations in OpenAlex.

  1. Does Basal Cell Carcinoma Arise from a Precursor Lesion?The Journal of investigative dermatology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. 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

4 authors at 2 institutions in 2 countries.

Yao YuanLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Natalia Salinas ParraLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Qianming ChenThe Affiliated Hospital of Stomatology, School of Stomatology, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Ramiro Iglesias-BartolomeLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: ramiro.iglesias-bartolome@nih.gov.
National Institutes of Health · USZhejiang University · CN

Funding

Signaling pathways regulating stem cell fate decisionsZIABC011763 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI IGLESIAS-BARTOLOME, RAMIRO · 2017 to 2025
$7.5M
G-protein-coupled receptor signaling in cancer development and treatmentZIABC011764 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI IGLESIAS-BARTOLOME, RAMIRO · 2017 to 2022
$1.9M
Intramural NIH HHS ZIA BC011763Intramural NIH HHS ZIA BC011764
6 · The paper itself

Abstract

Disruption of the transcriptional activity of the Hippo pathway members YAP1 and TAZ has become a major target for cancer treatment. However, detailed analysis of the effectiveness and networks affected by YAP1/TAZ transcriptional targeting is limited. In this study, we utilize TEAD inhibitor, an inhibitor of the binding of YAP1 and TAZ with their main transcriptional target TEAD in a mouse model of basal cell carcinoma, to unveil the consequences of YAP1/TAZ transcriptional blockage in cancer cells. Both TEAD inhibitor and YAP1/TAZ knockdown lead to reduced proliferation and increased differentiation of mouse basal cell carcinoma driven by oncogenic hedgehog-smoothened (SmoM2) activity. Although TEAD-transcriptional networks were essential to inactivate differentiation, this inactivation was found to be indirect and potentially mediated through the repression of KLF4 by SNAI2. By comparing the transcriptional effects of TEAD inhibition with those caused by YAP1/TAZ depletion, we determined YAP1/TAZ‒TEAD‒independent effects in cancer cells that impact STAT3 and NF-κB. Our results reveal the gene networks affected by targeting YAP1/TAZ‒TEAD in basal cell carcinoma tumors and expose the potential pitfalls for targeting TEAD transcription in cancer.

Indexed as

AnimalsBasal Cell CarcinomaCarcinogenesisCell DifferentiationCell Line, TumorDisease Models, AnimalGene Expression Regulation, NeoplasticGene Knockdown TechniquesHedgehogsHippo Signaling PathwayHumansKruppel-Like Factor 4MiceNF-kappa BSnail Family Transcription FactorsSTAT3 Transcription FactorKruppel-Like Factor 4NF-kappa BSnai2 protein, mouseSnail Family Transcription FactorsSTAT3 Transcription FactorTEA Domain Transcription FactorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID34293352
PMCPMC10292110
OpenAlexW3183426580

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.