TY - JOUR AU - Pastushenko, Ievgenia AU - Mauri, Federico AU - Song, Yura AU - de Cock, Florian AU - Meeusen, Bob AU - Swedlund, Benjamin AU - Impens, Francis AU - Van Haver, Delphi AU - Opitz, Matthieu AU - Thery, Manuel AU - Bareche, Yacine AU - Lapouge, Gaelle AU - Vermeersch, Marjorie AU - Van Eycke, Yves-Rémi AU - Balsat, Cédric AU - Decaestecker, Christine AU - Sokolow, Youri AU - Hassid, Sergio AU - Perez-Bustillo, Alicia AU - Agreda-Moreno, Beatriz AU - Rios-Buceta, Luis AU - Jaen, Pedro AU - Redondo, Pedro AU - Sieira-Gil, Ramon AU - Millan-Cayetano, Jose F AU - Sanmatrtin, Onofre AU - D'Haene, Nicky AU - Moers, Virginie AU - Rozzi, Milena AU - Blondeau, Jeremy AU - Lemaire, Sophie AU - Scozzaro, Samuel AU - Janssens, Veerle AU - De Troya, Magdalena AU - Dubois, Christine AU - Pérez-Morga, David AU - Salmon, Isabelle AU - Sotiriou, Christos AU - Helmbacher, Francoise AU - Blanpain, Cédric PY - 2020 DO - 10.1038/s41586-020-03046-1 UR - https://hdl.handle.net/10668/26673 T2 - Nature AB - FAT1, which encodes a protocadherin, is one of the most frequently mutated genes in human cancers1-5. However, the role and the molecular mechanisms by which FAT1 mutations control tumour initiation and progression are poorly understood. Here, using... LA - en KW - Adaptor Proteins, Signal Transducing KW - Animals KW - Cadherins KW - Carcinoma, Squamous Cell KW - Disease Progression KW - Enhancer of Zeste Homolog 2 Protein KW - Epithelial Cells KW - Epithelial-Mesenchymal Transition KW - Gene Deletion KW - Gene Expression Regulation, Neoplastic KW - Humans KW - Hyaluronan Receptors KW - Lung Neoplasms KW - Mesoderm KW - Mice KW - Neoplasm Metastasis KW - Neoplasms KW - Neoplastic Stem Cells KW - Phenotype KW - Phosphoproteins KW - Proteomics KW - SOXB1 Transcription Factors KW - Signal Transduction KW - Skin Neoplasms KW - Transcription Factors KW - YAP-Signaling Proteins KW - Zinc Finger E-box-Binding Homeobox 1 KW - src-Family Kinases TI - Fat1 deletion promotes hybrid EMT state, tumour stemness and metastasis. TY - research article VL - 589 ER -