ArticleCancer science2026
Resveratrol as a Novel YAP Inhibitor Targeting Glioblastoma Progression and Sensitizing to Chemotherapy.
Article in Cancer science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- Targeting Nectin-4 sensitizes glioblastoma to temozolomide.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Dysregulation of YAP, the terminal effector of the Hippo pathway, contributes to cancer progression and drug resistance. Its role in glioblastoma (GBM), the most aggressive brain cancer, remains incompletely understood. Single-cell RNA sequencing data from a published GBM dataset were reanalyzed to assess YAP expression across cell populations. YAP was silenced via shRNA in GBM cell lines (U-251 MG, U-87 MG) and patient-derived GBM cells. Resveratrol (RV), a natural blood-brain barrier-permeable compound, was evaluated for growth inhibition and YAP-targeted effects. Functional assays measured proliferation, spheroid formation, migration, invasion, and drug sensitivity. YAP and its cofactor TEAD were highly upregulated in GBM cells compared with normal brain and stromal cells. YAP depletion by shRNA suppressed proliferation, spheroid formation, migration, and invasion. RV treatment similarly inhibited YAP expression, reducing proliferation and viability in monolayer and 3D spheroid cultures, and impairing migration and invasion via epithelial-mesenchymal transition (EMT) inhibition. RV-mediated YAP suppression also enhanced sensitivity to temozolomide (TMZ) and carmustine (BCNU), increasing their cytotoxicity in GBM cells. RV acts as a novel YAP inhibitor in GBM, impairing malignant phenotypes and potentiating the effects of standard chemotherapy. These findings support RV as a potential adjunct in YAP-targeted GBM therapy, warranting further in vivo validation for clinical translation.
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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.