Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12779/6556
Title: Dbl oncogene expression in MCF-10 A epithelial cells disrupts mammary acinar architecture, induces EMT and angiogenic factor secretion
Authors: Vanni, Cristina
Ognibene, Marzia
Finetti, Federica 
Mancini, Patrizia 
Cabodi, Sara
Segalerba, Daniela
Torrisi, Maria Rosaria
DONNINI, SANDRA
Bosco, Maria Carla
Varesio, Luigi
Eva, Alessandra
Keywords: CCL2; Dbl oncogene; EMT; EMT, Epithelial-mesenchymal-transition; MCF-10 A; angiogenesis; migration; α-SMA, α-smooth muscle actin
Issue Date: 2015
Project: None 
Journal: CELL CYCLE
Abstract: 
The proteins of the Dbl family are guanine nucleotide exchange factors (GEFs) of Rho GTPases and are known to be involved in cell growth regulation. Alterations of the normal function of these proteins lead to pathological processes such as developmental disorders, neoplastic transformation, and tumor metastasis. We have previously demonstrated that expression of Dbl oncogene in lens epithelial cells modulates genes encoding proteins involved in epithelial-mesenchymal-transition (EMT) and induces angiogenesis in the lens. Our present study was undertaken to investigate the role of Dbl oncogene in epithelial cells transformation, providing new insights into carcinoma progression.To assess how Dbl oncogene can modulate EMT, cell migration, morphogenesis, and expression of pro-apoptotic and angiogenic factors we utilized bi- and 3-dimensional cultures of MCF-10 A cells. We show that upon Dbl expression MCF-10 A cells undergo EMT. In addition, we found that Dbl overexpression sustains Cdc42 and Rac activation inducing morphological alterations, characterized by the presence of lamellipodia and conferring a high migratory capacity to the cells. Moreover, Dbl expressing MCF-10 A cells form altered 3D structures and can induce angiogenesis by producing proangiogenic factors such as CCL2. These results support a role for Dbl oncogene in epithelial cell differentiation and transformation and suggest the relevance of GEF deregulation in tumor onset and progression.
Description: 
204559
URI: http://hdl.handle.net/20.500.12779/6556
ISSN: 1551-4005
DOI: 10.1080/15384101.2015.1021516
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