ArticleFEBS open bio2015
Small molecules inhibiting the nuclear localization of YAP/TAZ for chemotherapeutics and chemosensitizers against breast cancers.
Article in FEBS open bio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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.
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
112 citing papers in PubMed, 179 citations in OpenAlex.
- Targeting cancer signaling pathways and their therapeutic strategies.Discover oncology · 2026Review
- YAP1 Is a Crucial Nexus in the Tumor Microenvironment.Current medical science · 2026Review
- YAP1 Enhances Mesenchymal-Type Gene Expression in Human Adrenergic-Type Neuroblastoma Cells.Cancers · 2026Article
- NCAPH-YAP1 interaction promotes breast cancer stemness and tumor progression.Stem cell research & therapy · 2025Article
- Machine Learning Model for Predicting Sertraline-like Activities and Its Impact on Cancer Chemosensitization.ACS chemical neuroscience · 2025Article
- Pharmacological Dissection Identifies Retatrutide Overcomes the Therapeutic Barrier of Obese TNBC Treatments through Suppressing the Interplay between Glycosylation and Ubiquitylation of YAP.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Despicable role of epithelial-mesenchymal transition in breast cancer metastasis: ExhibitingCancer pathogenesis and therapy · 2025Review
- Targeting TEAD in cancer.Frontiers in oncology · 2025Review
- Identification of YAP regulators through high-throughput screening and NanoBiT-based validation-drug repositioning for cancer therapy.Animal cells and systems · 2025Article
- Review
- New Horizons in Cancer Progression and Metastasis:Biomedicines · 2024Review
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- The oncogenic axis YAP/MYC/EZH2 impairs PTEN tumor suppression activity enhancing lung tumorigenicity.Cell death discovery · 2024Article
- A highly sensitive reporter system to monitor endogenous YAP1/TAZ activity and its application in various human cells.Cancer science · 2024Article
- TPX2 overexpression promotes sensitivity to dasatinib in breast cancer by activating YAP transcriptional signaling.Molecular oncology · 2024Article
- TAZ is involved in breast cancer cell migration via regulating actin dynamics.Frontiers in oncology · 2024Article
- PPP1R12A is a recycling endosomal phosphatase that facilitates YAP activation.Scientific reports · 2023Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- Simvastatin Attenuates Glucocorticoid-Induced Human Trabecular Meshwork Cell Dysfunction via YAP/TAZ Inactivation.Current eye research · 2023Article
- New insights into the ambivalent role of YAP/TAZ in human cancers.Journal of experimental & clinical cancer research : CR · 2023Review
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YAP and TAZ oncoproteins confer malignancy and drug resistance to various cancer types. We screened for small molecules that inhibit the nuclear localization of YAP/TAZ. Dasatinib, statins and pazopanib inhibited the nuclear localization and target gene expression of YAP and TAZ. All three drugs induced phosphorylation of YAP and TAZ, and pazopanib induced proteasomal degradation of YAP/TAZ. The sensitivities to these drugs are correlated with dependence on YAP/TAZ in breast cancer cell lines. Combinations of these compounds with each other or with other anti-cancer drugs efficiently reduced cell proliferation of YAP/TAZ-dependent breast cancer cells. These results suggest that these drugs can be therapeutics and chemosensitizers for YAP/TAZ-dependent breast cancers.
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What Socratic holds
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 Socratic graph.