Arachidonic acid induces an increase of beta-1,4-galactosyltransferase I expression in MDA-MB-231 breast cancer cells

作者：Villegas Comonfort Socrates; Serna Marquez Nathalia; Galindo Hernandez Octavio; Navarro Tito Napoleon; Perez Salazar Eduardo

来源：Journal of Cellular Biochemistry, 2012, 113(11): 3330-3341.

DOI：10.1002/jcb.24209

• BREAST CANCER
• GALT I
• ARACHIDONIC ACID
• ADHESION

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 beta-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 PLA2a, 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. J. Cell. Biochem. 113: 33303341, 2012.

• 出版日期2012-11