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Int. J. Mol. Sci. 2016, 17(8), 1309; doi:10.3390/ijms17081309

ST6GALNAC5 Expression Decreases the Interactions between Breast Cancer Cells and the Human Blood-Brain Barrier

1
Université d’Artois (UArtois), EA2465, Laboratoire de la Barrière Hémato-Encéphalique (LBHE), Lens F-62300, France
2
Structural and Functional Glycobiology Unit, Unité Mixte de Recherche (UMR) du Centre National de la Recherche Scientifique (CNRS) 8576, University of Lille, Villeneuve d’Ascq F-59655, France
3
Cell Plasticity and Cancer, U908 INSERM, University of Lille, Villeneuve d’Ascq F-59655, France
*
Author to whom correspondence should be addressed.
Academic Editor: Cheorl-Ho Kim
Received: 25 June 2016 / Revised: 3 August 2016 / Accepted: 3 August 2016 / Published: 11 August 2016
(This article belongs to the Special Issue Glycan–Receptor Interaction)
View Full-Text   |   Download PDF [4002 KB, uploaded 11 August 2016]   |  

Abstract

The ST6GALNAC5 gene that encodes an α2,6-sialyltransferase involved in the biosynthesis of α-series gangliosides, was previously identified as one of the genes that mediate breast cancer metastasis to the brain. We have shown that the expression of ST6GALNAC5 in MDA-MB-231 breast cancer cells resulted in the expression of GD1α ganglioside at the cell surface. By using a human blood-brain barrier in vitro model recently developed, consisting in CD34+ derived endothelial cells co-cultivated with pericytes, we show that ST6GALNAC5 expression decreased the interactions between the breast cancer cells and the human blood-brain barrier. View Full-Text
Keywords: breast cancer; blood-brain barrier; gangliosides; GD1α; ST6GALNAC5; sialyltransferase; brain metastasis breast cancer; blood-brain barrier; gangliosides; GD1α; ST6GALNAC5; sialyltransferase; brain metastasis
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Drolez, A.; Vandenhaute, E.; Delannoy, C.P.; Dewald, J.H.; Gosselet, F.; Cecchelli, R.; Julien, S.; Dehouck, M.-P.; Delannoy, P.; Mysiorek, C. ST6GALNAC5 Expression Decreases the Interactions between Breast Cancer Cells and the Human Blood-Brain Barrier. Int. J. Mol. Sci. 2016, 17, 1309.

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