Journal article
β-arrestin1/YAP/mutant p53 complexes orchestrate the endothelin A receptor signaling in high-grade serous ovarian cancer
Abstract
The limited clinical response observed in high-grade serous ovarian cancer (HG-SOC) with high frequency of TP53 mutations (mutp53) might be related to mutp53-driven oncogenic pathway network. Here we show that β-arrestin1 (β-arr1), interacts with YAP, triggering its cytoplasmic-nuclear shuttling. This interaction allows β-arr1 to recruit mutp53 to the YAP-TEAD transcriptional complex upon activation of endothelin-1 receptors (ET-1R) in …
Authors
Tocci P; Cianfrocca R; Di Castro V; Rosanò L; Sacconi A; Donzelli S; Bonfiglio S; Bucci G; Vizza E; Ferrandina G
Journal
Nature Communications, Vol. 10, No. 1,
Publisher
Springer Nature
DOI
10.1038/s41467-019-11045-8
ISSN
2041-1723
Associated Experts
Fields of Research (FoR)
Medical Subject Headings (MeSH)
Adaptor Proteins, Signal TransducingAnimalsAntineoplastic AgentsCell Line, TumorCell SurvivalCystadenocarcinoma, SerousDisease Models, AnimalEndothelin-1FemaleGene Expression Regulation, NeoplasticGuanine Nucleotide Exchange FactorsHumansMice, NudeMutationOvarian NeoplasmsProtein Serine-Threonine KinasesPyrimidinesReceptor, Endothelin ASignal TransductionSulfonamidesTranscription FactorsTumor Suppressor Protein p53Xenograft Model Antitumor AssaysYAP-Signaling Proteinsbeta-Arrestin 1rho GTP-Binding ProteinsrhoA GTP-Binding Protein