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Title

Lysyl oxidase-like 2 (LOXL2), a new regulator of cell polarity required for metastatic dissemination of basal-like breast carcinomas

AuthorsMoreno-Bueno, Gema ; Salvador, Fernando ; Martín, Alberto ; Floristán, Alfredo; Cuevas, Eva P.; Santos, Vanesa ; Montes, Amalia; Morales, Saleta ; Castilla, María Ángeles; Portillo, Francisco ; Peinado, Héctor; Palacios Calvo, José ; Cano, Amparo
KeywordsBasal-like carcinomas
Breast cancer
EMT
LOXL2
Metastasis
Issue DateSep-2011
PublisherWiley-Blackwell
European Molecular Biology Organization
CitationEMBO Molecular Medicine 3(9): 528-544 (2011)
AbstractBasal-like breast carcinoma is characterized by the expression of basal/myoepithelial markers, undifferentiated phenotype, highly aggressive behaviour and frequent triple negative status (ESR−, PR−, Her2neu−). We have previously shown that epithelial–mesenchymal transition (EMT) occurs in basal-like breast tumours and identified Lysyl-oxidase-like 2 (LOXL2) as an EMT player and poor prognosis marker in squamous cell carcinomas. We now show that LOXL2 mRNA is overexpressed in basal-like human breast carcinomas. Breast carcinoma cell lines with basal-like phenotype show a specific cytoplasmic/perinuclear LOXL2 expression, and this subcellular distribution is significantly associated with distant metastatic incidence in basal-like breast carcinomas. LOXL2 silencing in basal-like carcinoma cells induces a mesenchymal-epithelial transition (MET) associated with a decrease of tumourigenicity and suppression of metastatic potential. Mechanistic studies indicate that LOXL2 maintains the mesenchymal phenotype of basal-like carcinoma cells by a novel mechanism involving transcriptional downregulation of Lgl2 and claudin1 and disorganization of cell polarity and tight junction complexes. Therefore, intracellular LOXL2 is a new candidate marker of basal-like carcinomas and a target to block metastatic dissemination of this aggressive breast tumour subtype.
Publisher version (URL)http://dx.doi.org/10.1002/emmm.201100156
URIhttp://hdl.handle.net/10261/42259
DOI10.1002/emmm.201100156
ISSN1757-4676
E-ISSN1757-4684
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(IBIS) Artículos
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