Decrease in Fas-induced apoptosis by the γ-secretase inhibitor is dependent on p75NTR in a glioblastoma cell line

Bessette,Barbara; Durand,Karine; Giraud,Stéphanie; Bégaud,Gaëlle; Mathonnet,Muriel; Lalloué,Fabrice

doi:10.3892/etm.2012.480

Decrease in Fas-induced apoptosis by the γ-secretase inhibitor is dependent on p75NTR in a glioblastoma cell line

Authors:
- Barbara Bessette
- Karine Durand
- Stéphanie Giraud
- Gaëlle Bégaud
- Muriel Mathonnet
- Fabrice Lalloué
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Affiliations: University of Limoges, EA3842, ‘Cellular Homeostasis and Pathology’, Faculty of Medicine, 87025 Limoges Cedex, France
Published online on: February 13, 2012 https://doi.org/10.3892/etm.2012.480
Pages: 873-877

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Abstract

p75NTR, a member of the tumor necrosis factor superfamily, plays a key role in numerous physiological processes, including cell survival or apoptosis. Yet, the associated signaling pathways remain poorly understood. Similar to Notch, γ-secretase cleavage is implicated in the p75NTR signaling pathway leading to nuclear translocation of the intracellular domain and cell death. Fas receptor activation was found to promote cell death apoptosis in several cell lines. The goal of this study was to determine the respective role of p75NTR and Notch in the resistance to Fas-induced apoptosis in the U-87 MG glioblastoma cell line. Using the γ-secretase inhibitor, we investigated the modulation of Fas-induced apoptosis dependent on p75NTR-Fas receptor interaction. Whereas the U-87 MG cells expressed the Fas receptor at the cell membrane, apoptosis induced by Fas activation was decreased by the γ-secretase inhibitor. These data suggest that γ-secretase is implicated in p75NTR and Fas interaction leading to cell death signaling.

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