YAP and β-Catenin Cooperate to Drive Oncogenesis in Basal Breast Cancer

Abstract Targeting cancer stem cells (CSC) can serve as an effective approach toward limiting resistance to therapies. While basal-like (triple-negative) breast cancers encompass with CSC features, rational therapies remain poorly established. We show here that the receptor tyrosine kinase Met promotes YAP activity in and find enhanced within population. Interfering delayed formation, prevented luminal basal transdifferentiation, reduced CSC. knockout mammary glands revealed a decrease β-catenin target genes, suggesting is required for nuclear activity. Mechanistically, interacted TEAD4 at gene regulatory elements. Proteomic patient data upregulation of signature cancers. Our findings demonstrate cancers, dependent on signaling controls program. These suggest targeting YAP/TEAD4/β-catenin complex offers potential therapeutic strategy eradicating CSCs Significance: cooperates regulate this interaction may be novel therapy patients cancer.