Protein N-glycosylation alteration and glycolysis inhibition both contribute to the antiproliferative action of 2-deoxyglucose in breast cancer cells.

Date publication

juillet 2018

Journal

Breast cancer research and treatment

Auteurs

Membres identifiés du Cancéropôle Est :
Pr FLAMENT Stéphane , Dr MAZERBOURG Sabine

Tous les auteurs :
Berthe A, Zaffino M, Muller C, Foulquier F, Houdou M, Schulz C, Bost F, De Fay E, Mazerbourg S, Flament S

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/29971627

Résumé

Cancer cells often elicit a higher glycolytic rate than normal cells, supporting the development of glycolysis inhibitors as therapeutic agents. 2-Deoxyglucose (2-DG) is used in this context due to its ability to compete with glucose. However, many studies do not take into account that 2-DG inhibits not only glycolysis but also N-glycosylation. Since there are limited publications on 2-DG mechanism of action in breast cancer, we studied its effects in breast cancer cell lines to determine the part played by glycolysis inhibition and N-linked glycosylation interference.

Mots clés

2-Deoxyglucose, Breast cancer, Endoplasmic reticulum stress, Glycolysis, N-Glycosylation

Référence

Breast Cancer Res. Treat.. 2018 Jul 3;: