The abstract is read at the publisher; the summary is JClub's.
YAP1-2 promotes a BRD4-associated LLPS-like nuclear assembly with TEAD and TAZ, enriched at candidate super-enhancers, linked to malignant progression in high-grade serous ovarian cancer and gastric cancer models.
- Why it matters: It remains unclear how specific YAP1 splice isoforms set malignant transcriptional states, and whether isoform-specific complexes can form condensate-like structures that sustain cancer phenotypes.
- What they did: The study identifies YAP1-2 as a driver isoform and shows YAP1-2–TAZ heterodimers with TEAD form BRD4-associated nuclear assemblies with LLPS-like properties; disrupting heterodimerization, TEAD binding, or BRD4 interaction reduces assembly formation and phenotypes.
- The result: Exon-6 exclusion increases YAP1-2-associated nuclear puncta, invasion, and therapeutic resistance in HGSOC and enhances intraperitoneal tumor progression in gastric cancer xenografts; in HGSOC specimens, YAP1-2 abundance, YAP1-BRD4 proximity, and nuclear YAP1 puncta associate with advanced stages.
The findingWhy it mattersWhat they didThe result
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