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Battina R
; Rahhal R
; Wellstein A
; Riegel AT
; Sharif GM
Front Oncol
2025[]; 15
(?): 1692512
PMID41347094
show ga
The Hippo pathway is dysregulated in many cancers, leading to pro-oncogenic
effects. The transcription factor TEAD plays a critical role in early
development, tissue homeostasis, and cell proliferation, and it binds to the
downstream Hippo pathway co-activators YAP and TAZ. Numerous studies have
examined the roles of YAP/TAZ and TEAD in cancer, with their activity frequently
linked to poor clinical prognosis. This review discusses how targeting TEAD
interactions with coregulators-most notably YAP and TAZ-represents a promising
therapeutic strategy in oncology. Several pharmacological agents have been
developed to disrupt the YAP/TAZ-TEAD complex, and many are currently being
evaluated for clinical applicability across diverse cancer types. We review
current knowledge on the structure and homology of TEAD, emphasizing the
protein-protein interfaces that mediate binding to YAP/TAZ and other cofactors.
Advances in understanding the YAP/TAZ-TEAD complex have informed the development
of diverse strategies to inhibit downstream transcription of key oncogenic target
genes. Finally, we highlight TEAD inhibitors currently in clinical trials,
outlining their mechanisms of action, associated adverse effects, and potential
impact on the future therapeutic landscape.
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