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VE-cadherin promotes vasculogenic mimicry by modulating kaiso-dependent gene expression

AuthorsDelgado-Bellido, Daniel; Fernández-Cortés, Mónica; Rodríguez, María Isabel; Serrano-Sáenz, Santiago; Carracedo, Arkaitz; García-Díaz, Ángel; Oliver, Francisco Javier
Issue DateFeb-2019
PublisherSpringer Nature
CitationCell Death and Differentiation
AbstractAberrant extra-vascular expression of VE-cadherin (VEC) has been observed in metastasis associated with vasculogenic mimicry (VM); however, the ultimate reason why non-endothelial VEC favors the acquisition of this phenotype is not established. In this study, we show that human malignant melanoma cells have a constitutively high expression of phoshoVEC (pVEC) at Y658; pVEC is a target of focal adhesion kinase (FAK) and forms a complex with p120-catenin and the transcriptional repressor kaiso in the nucleus. FAK inhibition enabled kaiso to suppress the expression of its target genes and enhanced kaiso recruitment to KBS-containing promoters. Finally we have found that ablation of kaiso-repressed genes WNT11 and CCDN1 abolished VM. Thus, identification of pVEC as a component of the kaiso transcriptional complex establishes a molecular paradigm that links FAK-dependent phosphorylation of VEC as a major mechanism by which ectopical VEC expression exerts its function in VM.
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