A self-sustaining endocytic-based loop promotes breast cancer plasticity leading to aggressiveness and pro-metastatic behavior

A self-sustaining endocytic-based loop promotes breast cancer plasticity leading to aggressiveness and pro-metastatic behavior

It is unclear if genetic alterations in endocytic proteins play a causal role in high incidence human cancers. Here, the authors report the oncogenic role of Epsin3 (EPN3) in breast cancer, and show EPN3 to drive tumorigenesis through induction of a partial epithelial mesenchymal transition state an...

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Autores principales: Irene Schiano Lomoriello, Giovanni Giangreco, Claudia Iavarone, Chiara Tordonato, Giusi Caldieri, Gaetana Serio, Stefano Confalonieri, Stefano Freddi, Fabrizio Bianchi, Stefania Pirroni, Giovanni Bertalot, Giuseppe Viale, Davide Disalvatore, Daniela Tosoni, Maria Grazia Malabarba, Andrea Disanza, Giorgio Scita, Salvatore Pece, Brian K. Pilcher, Manuela Vecchi, Sara Sigismund, Pier Paolo Di Fiore
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/13d80ead99db4faeaae47bea7bd4c693
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Sumario:It is unclear if genetic alterations in endocytic proteins play a causal role in high incidence human cancers. Here, the authors report the oncogenic role of Epsin3 (EPN3) in breast cancer, and show EPN3 to drive tumorigenesis through induction of a partial epithelial mesenchymal transition state and a TGFβ-dependent regulatory loop that promotes cellular plasticity and invasive behaviour.

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