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Article

Verotoxin-1-Induced ER Stress Triggers Apoptotic or Survival Pathways in Burkitt Lymphoma Cells

1
UMR 8126 CNRS, Institut Gustave Roussy, Université Paris-Saclay, 94805 Villejuif, France
2
UMR 7592 CNRS, Institut Jacques Monod, Université Paris Diderot-Paris 7, 75205 Paris CEDEX 13, France
3
UMR 8200 CNRS, Institut Gustave Roussy, Université Paris-Saclay, 94805 Villejuif, France
4
INSERM U1279, Institut Gustave Roussy, Université Paris-Saclay, 94805 Villejuif, France
*
Authors to whom correspondence should be addressed.
Current adress: UMR 9018, Université Paris-Saclay, Institut Gustave Roussy, 94805 Villejuif, France.
Received: 10 April 2020 / Revised: 6 May 2020 / Accepted: 7 May 2020 / Published: 11 May 2020
(This article belongs to the Special Issue Toxins and Cancer Therapy)
Shiga toxins (Stxs) expressed by the enterohaemorrhagic Escherichia coli and enteric Shigella dysenteriae 1 pathogens are protein synthesis inhibitors. Stxs have been shown to induce apoptosis via the activation of extrinsic and intrinsic pathways in many cell types (epithelial, endothelial, and B cells) but the link between the protein synthesis inhibition and caspase activation is still unclear. Endoplasmic reticulum (ER) stress induced by the inhibition of protein synthesis may be this missing link. Here, we show that the treatment of Burkitt lymphoma (BL) cells with verotoxin-1 (VT-1 or Stx1) consistently induced the ER stress response by activation of IRE1 and ATF6—two ER stress sensors—followed by increased expression of the transcription factor C/REB homologous protein (CHOP). However, our data suggest that, although ER stress is systematically induced by VT-1 in BL cells, its role in cell death appears to be cell specific and can be the opposite: ER stress may enhance VT-1-induced apoptosis through CHOP or play a protective role through ER-phagy, depending on the cell line. Several engineered Stxs are currently under investigation as potential anti-cancer agents. Our results suggest that a better understanding of the signaling pathways induced by Stxs is needed before using them in the clinic. View Full-Text
Keywords: shiga toxins; Gb3/CD77; apoptosis; ER stress; autophagy; Burkitt lymphoma shiga toxins; Gb3/CD77; apoptosis; ER stress; autophagy; Burkitt lymphoma
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MDPI and ACS Style

Debernardi, J.; Pioche-Durieu, C.; Le Cam, E.; Wiels, J.; Robert, A. Verotoxin-1-Induced ER Stress Triggers Apoptotic or Survival Pathways in Burkitt Lymphoma Cells. Toxins 2020, 12, 316. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12050316

AMA Style

Debernardi J, Pioche-Durieu C, Le Cam E, Wiels J, Robert A. Verotoxin-1-Induced ER Stress Triggers Apoptotic or Survival Pathways in Burkitt Lymphoma Cells. Toxins. 2020; 12(5):316. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12050316

Chicago/Turabian Style

Debernardi, Justine, Catherine Pioche-Durieu, Eric Le Cam, Joëlle Wiels, and Aude Robert. 2020. "Verotoxin-1-Induced ER Stress Triggers Apoptotic or Survival Pathways in Burkitt Lymphoma Cells" Toxins 12, no. 5: 316. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12050316

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