ArticleNature communications2022
Pharmacological blockade of TEAD-YAP reveals its therapeutic limitation in cancer cells.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
What it found
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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
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- Dampened Regulatory Circuitry of TEAD1/ITGA1/ITGA2 Promotes TGFβ1 Signaling to Orchestrate Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Pooled it
- Emergence of invasiveGut microbes · 2026Article
- Sodium Butyrate Attenuates Doxorubicin Sardiotoxicity Through GPR41/GPR43-Sox4-PI3K/Akt Signaling.Cardiovascular toxicology · 2026Article
- YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling.Journal of cardiovascular translational research · 2026Review
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- Transcription factor targeting strategies in cancer: mechanisms, challenges and cutting-edge progress.Acta pharmacologica Sinica · 2026Review
- TEAD inhibitor induced switch in energy metabolism drives human podocyte injury in vitro.Archives of toxicology · 2026Article
- Covalent pan-TEAD inhibitors block YAP activity and demonstrate brain penetrance in a Hippo-dependent cancer model.Nature communications · 2026Article
- The Hippo signaling pathway in pediatric brain tumors: molecular mechanisms and therapeutic opportunities.Cancer metastasis reviews · 2026Review
- Drug resistant cancer cells show increased nuclear mechanotransduction and mechanically targetable YAP-regulated vulnerability.Biomaterials · 2026Article
- PIK3CA mutant cervical cancer is selectively suppressed by PI3Kα inhibition (Alpelisib/BYL-719 and Inavolisib/GDC-0077) and cooperates with HPV directed T cell therapy.Neoplasia (New York, N.Y.) · 2026Article
- Article
- Targeting Autophagy to Overcome Chemoresistance and Immune Resistance in Triple-Negative Breast Cancer.Cancers · 2026Review
- Hippo-YAP/TAZ Signaling in Astrocytes and Microglia: Role in Neuroinflammation, Neurodegeneration and Glial Tumors.International journal of molecular sciences · 2026Review
- Targeting cancer signaling pathways and their therapeutic strategies.Discover oncology · 2026Review
- Extracellular vesicles conjugated with c(RGDyk) peptide targeting integrin αVβ3 repair optic nerve injury through YAP/TAZ and Smad2/3 signaling.Stem cells translational medicine · 2026Article
- Combination of YAP inhibition and photodynamic therapy induces dual DNA damage and activates STING pathway to enhance immunotherapy in uveal melanoma.Redox biology · 2026Article
- YAP1 Is a Crucial Nexus in the Tumor Microenvironment.Current medical science · 2026Review
- Functional Difference of MYC and MYCN in Combined Hepatocellular-Cholangiocarcinoma: Regulation of Differentiation by HNF1B.Cancer science · 2026Article
- A Three-subtype Molecular model of Cervical Cancer: Multiple PI3K Pathway inhibitors suppress growth and cooperate with HPV-directed immunotherapy.medRxiv : the preprint server for health sciences · 2026Article
16 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
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Targeting TEAD autopalmitoylation has been proposed as a therapeutic approach for YAP-dependent cancers. Here we show that TEAD palmitoylation inhibitor MGH-CP1 and analogues block cancer cell "stemness", organ overgrowth and tumor initiation in vitro and in vivo. MGH-CP1 sensitivity correlates significantly with YAP-dependency in a large panel of cancer cell lines. However, TEAD inhibition or YAP/TAZ knockdown leads to transient inhibition of cell cycle progression without inducing cell death, undermining their potential therapeutic utilities. We further reveal that TEAD inhibition or YAP/TAZ silencing leads to VGLL3-mediated transcriptional activation of SOX4/PI3K/AKT signaling axis, which contributes to cancer cell survival and confers therapeutic resistance to TEAD inhibitors. Consistently, combination of TEAD and AKT inhibitors exhibits strong synergy in inducing cancer cell death. Our work characterizes the therapeutic opportunities and limitations of TEAD palmitoylation inhibitors in cancers, and uncovers an intrinsic molecular mechanism, which confers potential therapeutic resistance.
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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.