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

Justine Debernardi1, Catherine Pioche-Durieu2, Eric Le Cam3

  • 1UMR 8126 CNRS, Institut Gustave Roussy, Université Paris-Saclay, 94805 Villejuif, France.

Toxins
|May 15, 2020
PubMed

Insights

Shiga toxins (Stxs) inhibit protein synthesis, causing endoplasmic reticulum (ER) stress. This ER stress can either promote or protect against Stx-induced cell death, depending on the cell type.

Area of Science:

  • Microbiology and Molecular Biology
  • Cellular Biology
  • Toxicology

Background:

  • Shiga toxins (Stxs) from E. coli and Shigella dysenteriae 1 are protein synthesis inhibitors.
  • Stxs induce apoptosis, but the link between protein synthesis inhibition and caspase activation is unclear.
  • Endoplasmic reticulum (ER) stress is a potential mediator linking protein synthesis inhibition to cell death.

Purpose of the Study:

  • To investigate the role of ER stress in Shiga toxin-induced cell death.
  • To elucidate the signaling pathways involved in Stx-induced apoptosis.
  • To assess the potential of Stxs as anti-cancer agents.

Main Methods:

  • Treatment of Burkitt lymphoma (BL) cells with verotoxin-1 (VT-1 or Stx1).
  • Analysis of ER stress response markers, including IRE1, ATF6, and CHOP expression.
  • Evaluation of cell death pathways and ER-phagy.

Main Results:

  • VT-1 consistently induced ER stress in BL cells, activating IRE1 and ATF6 and increasing CHOP expression.
  • ER stress played a cell-specific role in VT-1-induced cell death, either enhancing apoptosis via CHOP or providing protection through ER-phagy.
  • The impact of ER stress on cell death was dependent on the specific cell line.

Conclusions:

  • ER stress is a key component of the cellular response to Shiga toxins.
  • The role of ER stress in Stx-induced apoptosis is complex and cell-type dependent.
  • Further research into Stx signaling pathways is crucial for their potential clinical application, particularly as anti-cancer agents.
Keywords:
Burkitt lymphomaER stressGb3/CD77apoptosisautophagyshiga toxins

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