Journal
DEVELOPMENTAL CELL
Volume 30, Issue 5, Pages 553-568Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2014.08.006
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Funding
- Fonds de Recherche du Quebec-Sante
- Fondazione Umberto Veronesi
- Associazione Italiana per la Ricerca sul Cancro [10168]
- Associazione Italiana per la Ricerca sul Cancro (START UP program)
- Italian Ministry of Health
- Association for International Cancer Research [AICR 09-0582]
- CARIPLO Foundation
- European Research Council [268836]
- Fondazione Piemontese per la Ricerca sul Cancro-ONLUS [5X1000 2008]
- Italian Ministry of Education [MIUR-PRIN-2009X23L78]
- Italian Ministry of University and Research [MIUR-PRIN-2009X23L78]
- [2010-0737]
- [2011-0596]
- European Research Council (ERC) [268836] Funding Source: European Research Council (ERC)
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The role of endocytic proteins and the molecular mechanisms underlying epithelial cell cohesion and tumor dissemination are not well understood. Here, we report that the endocytic F-BAR-containing CDC42-interacting protein 4 (CIP4) is required for ERBB2-and TGF-beta 1-induced cell scattering, breast cancer (BC) cell motility and invasion into 3D matrices, and conversion from ductal breast carcinoma in situ to invasive carcinoma in mouse xenograft models. CIP4 promotes the formation of an E-cadherin-CIP4-SRC complex that controls SRC activation, E-cadherin endocytosis, and localized phosphorylation of the myosin light chain kinase, thereby impinging on the actomyosin contractility required to generate tangential forces to break cell-cell junctions. CIP4 is upregulated in ERBB2-positive human BC, correlates with increased distant metastasis, and is an independent predictor of poor disease outcome in subsets of BC patients. Thus, it critically controls cell-cell cohesion and is required for the acquisition of an invasive phenotype in breast tumors.
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