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Glycobiology Advance Access originally published online on February 24, 2009
Glycobiology 2009 19(6):576-582; doi:10.1093/glycob/cwp015
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Published by Oxford University Press 2009.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/ by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Different mechanisms are involved in apoptosis induced by melanoma gangliosides on human monocyte-derived dendritic cells

Karim Bennaceur1,2,3, Iuliana Popa2,5, Jessica Alice Chapman4, Camille Migdal2, Josette Péguet-Navarro2, Jean-Louis Touraine3 and Jacques Portoukalian2

2 Laboratory of Dermatological Research, University of Lyon-1 EA 41-69, Building R, Edouard Herriot Hospital, 69437 Lyon Cx 03, France
3 Department of Transplantation and Clinical Immunology, University of Lyon-1 and Edouard Herriot Hospital, Lyon, France
4 Faculty of Life Sciences, University of Manchester, UK
5 Institute of Macromolecular Chemistry Petru Poni, Iasi, Romania

1 To whom correspondence should be addressed: e-mail: karim.bennaceur{at}newcastle.ac.uk

Received on May 16, 2008; revised on February 4, 2009; accepted on February 6, 2009

Tumor escape is linked to multiple mechanisms, notably the liberation, by tumor cells, of soluble factors that inhibit the function of dendritic cells (DC). We have shown that melanoma gangliosides impair DC differentiation and induce their apoptosis. The present study was aimed to give insight into the mechanisms involved. DC apoptosis was independent of the catabolism of gangliosides since lactosylceramide did not induce cell death. Apoptosis induced by GM3 and GD3 gangliosides was not blocked by inhibitors of de novo ceramide biosynthesis, whereas the acid sphingomyelinase inhibitor desipramine only prevented apoptosis induced by GM3. Furthermore, our results suggest that DC apoptosis was triggered via caspase activation, and it was ROS dependent with GD3 ganglioside, suggesting that GM3 and GD3 induced apoptosis through different mechanisms.

Key words: acid sphingomyelinase / apoptosis / ceramides / dendritic cells / gangliosides / melanoma


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