ArticleNature communications2016
A splicing isoform of TEAD4 attenuates the Hippo-YAP signalling to inhibit tumour proliferation.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 76 citations in OpenAlex.
- RBM25 Drives Hepatocellular Carcinoma Progression by Stabilizing YAP Through Regulating Oncogenic Splicing-switch of MYPT1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Marine-Derived Fungal Metabolite MHO7 Promotes Breast Cancer Apoptosis as a Hippo Pathway Regulator by Modulating the YAP-TEAD Axis.Marine drugs · 2026Article
- CircSPARC promotes esophageal squamous cell carcinoma through an HNRNPC-EPN2 splicing axis that activates Wnt/β-Catenin signaling.Molecular cancer · 2026Article
- The bidirectional interplay between RNA processing and mechanotransduction.Cell reports · 2025Review
- Hippo Pathway Dysregulation in Thymic Epithelial Tumors (TETs): Associations with Clinicopathological Features and Patients' Prognosis.International journal of molecular sciences · 2025Article
- Dual Disruption of EGFR/PI3K Signaling: IGF2BP2 Targeting Reverses Anti-EGFR Resistance in CAFs-Infiltrated Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- The cryptic lncRNA-encoded microprotein TPM3P9 drives oncogenic RNA splicing and tumorigenesis.Signal transduction and targeted therapy · 2025Article
- Alternative splicing of EZH2 regulated by SNRPB mediates hepatocellular carcinoma progression via BMP2 signaling pathway.iScience · 2025Article
- Identification and validation of protein biomarkers for predicting gastrointestinal stromal tumor recurrence.Computational and structural biotechnology journal · 2024Article
- The role of TEAD4 in trophectoderm commitment and development is not conserved in non-rodent mammals.Development (Cambridge, England) · 2024Article
- Radiation-induced YAP/TEAD4 binding confers non-small cell lung cancer radioresistance via promoting NRP1 transcription.Cell death & disease · 2024Article
- Integrative Epigenetic and Molecular Analysis Reveals a Novel Promoter for a New Isoform of the Transcription Factor TEAD4.International journal of molecular sciences · 2024Article
- The function of alternative splicing in the proteome: rewiring protein interactomes to put old functions into new contexts.Nature structural & molecular biology · 2023Review
- Article
- RBM4 dictates ESCC cell fate switch from cellular senescence to glutamine-addiction survival through inhibiting LKB1-AMPK-axis.Signal transduction and targeted therapy · 2023Article
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- RBM4 regulates cellular senescence via miR1244/SERPINE1 axis.Cell death & disease · 2023Article
- Loss of RBMS1 promotes anti-tumor immunity through enabling PD-L1 checkpoint blockade in triple-negative breast cancer.Cell death and differentiation · 2022Article
- RBFOX2-regulated TEAD1 alternative splicing plays a pivotal role in Hippo-YAP signaling.Nucleic acids research · 2022Article
- Chicken CDS2 isoforms presented distinct spatio-temporal expression pattern and regulated by insulin in a breed-specific manner.Poultry science · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Aberrant splicing is frequently found in cancer, yet the biological consequences of such alterations are mostly undefined. Here we report that the Hippo-YAP signalling, a key pathway that regulates cell proliferation and organ size, is under control of a splicing switch. We show that TEAD4, the transcription factor that mediates Hippo-YAP signalling, undergoes alternative splicing facilitated by the tumour suppressor RBM4, producing a truncated isoform, TEAD4-S, which lacks an N-terminal DNA-binding domain, but maintains YAP interaction domain. TEAD4-S is located in both the nucleus and cytoplasm, acting as a dominant negative isoform to YAP activity. Consistently, TEAD4-S is reduced in cancer cells, and its re-expression suppresses cancer cell proliferation and migration, inhibiting tumour growth in xenograft mouse models. Furthermore, TEAD4-S is reduced in human cancers, and patients with elevated TEAD4-S levels have improved survival. Altogether, these data reveal a splicing switch that serves to fine tune the Hippo-YAP pathway.
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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.