Evidence map›Paper›PMID 36285644›Full record

ArticleMolecular carcinogenesis2023

Sulforaphane inhibits CD44v6/YAP1/TEAD signaling to suppress the cancer phenotype.

Xi Chen, Gautam Adhikary, Emily Ma, John J Newland, Warren Naselsky, Wen Xu, Richard L Eckert

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. CSCScientific reports · 2024
    Article
  7. Sulforaphane activates CD8Journal for immunotherapy of cancer · 2024
    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

7 authors at 1 institution in 1 country.

Xi ChenDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Gautam AdhikaryDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Emily MaDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
John J NewlandDivision of Thoracic Oncology, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Warren NaselskyDivision of Thoracic Oncology, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Wen XuDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Richard L EckertDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-3770-4779
University of Maryland, Baltimore · US

Funding

UNIVERSITY OF MARYLAND GREENEBAUM CANCER CENTERSUPPORT GRANTP30CA134274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI Vu H. Duong · 2008 to 2026
$51.0M
Training Grant in Cancer BiologyT32CA154274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI Toni M Antalis, CURT I CIVIN · 2011 to 2026
$6.8M
A novel sulforaphane cancer preventionmechanismR01CA211909 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI ECKERT, RICHARD L. · 2018 to 2022
$2.1M
NCI NIH HHS P30 CA134274NCI NIH HHS R01 CA211909NCI NIH HHS T32 CA154274
6 · The paper itself

Abstract

Sulforaphane (SFN) is a promising cancer prevention and treatment agent that strongly suppresses the cutaneous squamous cell carcinoma (CSCC) cell cancer phenotype. We previously showed that yes-associated protein 1 (YAP1)/TEAD signaling is a key procancer stimulator of the aggressive CSCC cell cancer phenotype. However, SFN-responsive upstream regulators of YAP1/TEAD signaling are not well characterized and so there is a pressing need to identify these factors. We show that CD44v6 knockdown reduces YAP1/TEAD-dependent transcription and target gene expression, and that this is associated with reduced spheroid formation, invasion and migration. CD44v6 knockout cell lines also display reduced YAP1/TEAD activity and target gene expression and attenuated spheroid formation, invasion, migration and tumor formation. An important finding is that SFN treatment suppresses CD44v6 level leading to a reduction in YAP1/TEAD signaling and marker gene expression. Sox2 level and epithelial-mesenchymal transition (EMT) are also reduced. Forced expression of constitutive active YAP1 in CD44v6 knockdown cells partially restores the aggressive cancer phenotype. These important findings suggest that CD44v6 drives YAP1/TEAD signaling to enhance the CSCC cell cancer phenotype and that SFN treatment reduces CD44v6 level/function which, in turn, reduces YAP1/TEAD signaling leading to reduced stemness, EMT and tumor growth.

Indexed as

Carcinoma, Squamous CellSkin NeoplasmsAdaptor Proteins, Signal TransducingCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsIsothiocyanatesSulfoxidesTranscription FactorsAdaptor Proteins, Signal TransducingCD44v6 antigenHyaluronan ReceptorsIsothiocyanatessulforaphaneSulfoxidesTranscription Factorscancer preventionCD44v6squamous cell carcinomasulforaphaneYAP1/TEAD signaling

Identifiers

PMID36285644
PMCPMC9851963
OpenAlexW4307341695

What OpenQuestion 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 OpenQuestion graph.