ArticleMolecular carcinogenesis2023
Sulforaphane inhibits CD44v6/YAP1/TEAD signaling to suppress the cancer phenotype.
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.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Sulforaphane-Activated Functional Nucleic Acids for Cancer Therapy: Mechanisms, Delivery Strategies, and Nanomedicine Advances.International journal of molecular sciences · 2026Review
- Sulforaphane as a Multi-Scale Mechano-Modulator in Cancer: An Integrative Perspective.Biology · 2026Article
- Multidimensional Regulatory Network ofOncology research · 2026Review
- Engineering Mechanical Microenvironments: Integration of Substrate and Flow Mechanics Reveals the Impact on the Endothelial Glycocalyx.ACS biomaterials science & engineering · 2025Article
- Potential mechanisms of cancer prevention and treatment by sulforaphane, a natural small molecule compound of plant-derived.Molecular medicine (Cambridge, Mass.) · 2024Review
- CSCScientific reports · 2024Article
- Sulforaphane activates CD8Journal for immunotherapy of cancer · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
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.