TEAD1
Overview
TEAD1 encodes a TEA domain transcription factor that is the primary nuclear effector of YAP1 and WWTR1 (TAZ) in the Hippo pathway. In gallbladder cancer, TEAD1 mediates stiffness-induced transcriptional activation of SEMA7A in cancer-associated fibroblasts by binding the SEMA7A promoter under high-stiffness conditions.
Alterations observed in the corpus
- ChIP confirmed TEAD1 binding at the SEMA7A promoter in primary gallbladder fibroblasts, with enrichment under 16 kPa vs 0.5 kPa stiffness conditions; mechanistically downstream of YAP1/WWTR1 mechanotransduction. PMID:24997986
Cancer types (linked)
- Gallbladder cancer (GBC): TEAD1 acts as the transcriptional node linking mechanical stiffness (via YAP1/WWTR1) to SEMA7A-driven paracrine tumor promotion. PMID:24997986
Co-occurrence and mutual exclusivity
- Functions as part of the YAP1/WWTR1/TEAD1 mechanotransduction complex; verteporfin disrupts YAP1–TEAD1 interaction and abolishes SEMA7A induction. PMID:24997986
Therapeutic relevance
- Indirect target: verteporfin blocks YAP–TEAD interaction, abolishing stiffness-induced SEMA7A secretion and downstream tumor-promoting effects in GBC models. PMID:24997986
Open questions
- Somatic mutations or copy number changes in TEAD1 were not profiled in the citing GBC study, which focuses on expression and protein-level mechanosignaling.
Sources
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