ReviewCancer biology & therapy2013
Emerging roles of TEAD transcription factors and its coactivators in cancers.
Review in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed.
- Two distinct modes of Vgll4-mediated Tead regulation control organ size in zebrafish.Communications biology · 2026Article
- Development and validation of a novel senescence-associated gene signature for prediction of survival and endocrine-disrupting chemicals in bladder cancer.Discover oncology · 2026Article
- Hippo pathway effectors are associated with glioma patient survival, control cell proliferation and sterol metabolism through TEAD3.Brain pathology (Zurich, Switzerland) · 2025Article
- Transcriptional Condensates: Epigenetic Reprogramming and Therapeutic Targets in Hematologic Malignancies.Cancers · 2025Review
- Single-cell transcriptomic analysis reveals metastatic and immunosuppressive characteristics in meningioma brain-tumor interface.Journal of translational medicine · 2025Article
- TEAD4 Transcriptionally Activates TRIB3 to Induce Ferroptosis Resistance through the MEK/ERK Signaling Pathway in Colorectal Cancer.Gut and liver · 2025Article
- Advancements of anticancer agents by targeting the Hippo signalling pathway: biological activity, selectivity, docking analysis, and structure-activity relationship.Molecular diversity · 2025Review
- TEAD4 promoted proliferation and metastasis of gallbladder cancer by regulation of TMPRSS4.Clinical & experimental metastasis · 2025Article
- YAP/TAZ Inhibitor-Based Drug Delivery System for Selective Tumor Accumulation and Cancer Combination Therapy.Biomacromolecules · 2025Article
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- Article
- Aggressive high-grade NF2 mutant meningiomas downregulate oncogenic YAP signaling via the upregulation of VGLL4 and FAT3/4.bioRxiv : the preprint server for biology · 2024Article
- SUMOylation of TEAD1 Modulates the Mechanism of Pathological Cardiac Hypertrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
- YAP1 expression in colorectal cancer confers the aggressive phenotypes via its target genes.Cell cycle (Georgetown, Tex.) · 2024Article
- Hippo Signaling Mediates TGFβ-Dependent Transcriptional Inputs in Cardiac Cushion Mesenchymal Cells to Regulate Extracellular Matrix Remodeling.Journal of cardiovascular development and disease · 2023Article
- Review
- Development and characterization of a recombinant silk network for 3D culture of immortalized and fresh tumor-derived breast cancer cells.Bioengineering & translational medicine · 2023Article
- Nuclear proinflammatory cytokine S100A9 enhances expression of human papillomavirus oncogenes via transcription factor TEAD1.Journal of virology · 2023Article
- TEAD4 predicts poor prognosis and transcriptionally targets PLAGL2 in serous ovarian cancer.Human cell · 2023Article
76 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TEAD proteins are transcription factors that are crucial for development, but also play a role in cancers. Several developmentally and pathologically important genes are upregulated by TEADs. TEADs have a TEA domain that enables them to bind specific DNA elements and a transactivation domain that enables them to interact with coactivators. TEADs on their own are unable to activate transcription and they require the help of coactivators. Several TEAD-interacting coactivators are known and they can be classified into three groups: (1) YAP and its paralog TAZ; (2) Vgll proteins; and (3) p160s. Accordingly, these coactivators also play a role in development and cancers. Recent studies have shown that TEADs and their coactivators aid in the progression of various cancers, including the difficult to treat glioblastoma, liver and ovarian cancers. They facilitate cancer progression through expression of proliferation promoting genes such as c-myc, survivin, Axl, CTGF and Cyr61. There is also a good correlation between high TEAD or its coactivator expression and poor prognosis in various cancers. Given the fact that TEADs and their coactivators need to work together for a functional outcome, disrupting the interaction between them appears to be a viable option for cancer therapy. Structures of TEAD-coactivator complexes have been elucidated and will facilitate drug design and development.
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