Functional genomic screens uncover FERMT2 as a critical regulator of YAP/TAZ-driven tumorigenicity - PubMed
4 days ago
- #YAP/TAZ
- #FERMT2
- #Breast Cancer
- YAP and TAZ are transcriptional regulators involved in mechanotransduction, development, and tissue homeostasis, with dysregulation linked to cancer.
- CRISPR/Cas9-based screens identified FERMT2 as a critical regulator of YAP/TAZ-driven tumorigenicity in breast cancer cells.
- FERMT2, part of the integrin signaling pathway, is essential for YAP/TAZ-dependent fitness and tumorigenicity in triple-negative breast cancer.
- FERMT2 loss impairs YAP/TAZ nuclear accumulation, reduces target gene expression, and decreases phosphorylation at key tyrosine residues.
- FERMT2 regulates YAP/TAZ independently of the Hippo pathway through integrin-mediated FAK activation.
- Glucocorticoid-driven FAK activation can restore YAP/TAZ signaling in FERMT2-depleted cells.
- FERMT2 modulates actin-dependent regulation of YAP/TAZ, suggesting it as a potential therapeutic target in cancers with elevated YAP/TAZ signaling.