Arachidonic acid induces an increase of ß-1,4-galactosyltransferase I expression in MDA-MB-231 breast cancer cells.
J Cell Biochem
; 113(11): 3330-41, 2012 Nov.
Article
em En
| MEDLINE
| ID: mdl-22644815
ABSTRACT
Arachidonic acid (AA) is a common dietary n-6 cis polyunsaturated fatty acid that under physiological conditions is present in an esterified form in cell membrane phospholipids, and it might be present in the extracellular microenvironment. AA and its metabolites are implicated in FAK activation and cell migration in MDA-MB-231 breast cancer cells, and an epithelial-to-mesenchymal-like transition process in mammary non-tumorigenic epithelial cells MCF10A. During malignant transformation is present an altered expression of glycosiltransferases, which promote changes on the glycosilation of cell-surface proteins. The ß-1,4-galactosyltransferase I (GalT I) is an enzyme that participates in a variety of biological functions including cell growth, migration, and spreading. However, the participation of AA in the regulation of GalT I expression and the role of this enzyme in the cell adhesion process in breast cancer cells remains to be investigated. In the present study, we demonstrate that AA induces an increase of GalT I expression through a PLA2α, Src, ERK1/2, and LOXs activities-dependent pathway in MDA-MB-231 breast cancer cells. Moreover, MDA-MB-231 cells adhere to laminin via GalT I expression and pretreatment of cells with AA induces an increase of cell adhesion to laminin. In conclusion, our findings demonstrate, for the first time, that AA promotes an increase of GalT I expression through an AA metabolism, Src and ERK1/2 activities-dependent pathway, and that GalT I plays a pivotal role in cell adhesion to laminin in MDA-MB-231 breast cancer cells.
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Neoplasias da Mama
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Carcinoma
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Regulação Neoplásica da Expressão Gênica
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Ácido Araquidônico
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Galactosiltransferases
Limite:
Female
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Humans
Idioma:
En
Revista:
J Cell Biochem
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
México