ArticleThe EMBO journal2024
A non-canonical repressor function of JUN restrains YAP activity and liver cancer growth.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Elucidating the beneficial effects of gut microbiota-derived metabolites in treating hepatocellular carcinoma: an integrated network pharmacology, molecular docking, and single-cell sequencing analysis.Bioresources and bioprocessing · 2026Article
- Extracellular matrix reprogramming by the YAP/TAZ/TGF-β2 axis drives immune exclusion in cholangiocarcinoma models.The Journal of clinical investigation · 2026Article
- Embryonic Phase Transition/Separation on Hepatic Liquid Crystal Droplets Is Essential for Liver Development.Biology · 2026Article
- Positive TAZ-TDG feedback loop drives proneural-to-mesenchymal transition to promote glioblastoma progression.Journal of translational medicine · 2026Article
- Dual inhibition of glycolysis and glutaminolysis by targeting FOXO3 for hepatocellular carcinoma treatment.Oncogene · 2026Article
- Repurposing melatonin for its potential roles in gastrointestinal cancers: highlighting the molecular mechanisms.Cancer cell international · 2026Review
- Article
- New Roles of bZIP-Containing Membrane-Bound Transcription Factors in Chromatin Tethering and Karyoptosis.International journal of molecular sciences · 2025Review
- CAFs activated by YAP1 upregulate cancer matrix stiffness to mediate hepatocellular carcinoma progression.Journal of translational medicine · 2025Article
- Hippo/YAP signaling pathway in colorectal cancer: regulatory mechanisms and potential drug exploration.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Yes-associated protein (YAP) and its homolog, transcriptional coactivator with PDZ-binding motif (TAZ), are the main transcriptional downstream effectors of the Hippo pathway. Decreased Hippo pathway activity leads to nuclear translocation of YAP/TAZ where they interact with TEAD transcription factors to induce target gene expression. Unrestrained YAP/TAZ activity can lead to excessive growth and tumor formation in a short time, underscoring the evolutionary need for tight control of these two transcriptional coactivators. Here, we report that the AP-1 component JUN acts as specific repressor of YAP/TAZ at joint target sites to decrease YAP/TAZ activity. This function of JUN is independent of its heterodimeric AP-1 partner FOS and the canonical AP-1 function. Since expression of JUN is itself induced by YAP/TAZ, our work identifies a JUN-dependent negative feedback loop that buffers YAP/TAZ activity at joint genomic sites. This negative feedback loop gets disrupted in liver cancer to unlock the full oncogenic potential of YAP/TAZ. Our results thus demonstrate an additional layer of control for the interplay of YAP/TAZ and AP-1.
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