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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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IRE1 RNase controls CD95-mediated cell death.

Diana Pelizzari-Raymundo1,2, Victoria Maltret1,2, Manon Nivet1,2

  • 1Inserm U1242, University of Rennes, Rennes, France.

EMBO Reports
|February 22, 2024
PubMed
Summary
This summary is machine-generated.

The unfolded protein response sensor IRE1 regulates CD95/Fas death receptor expression and function in cancer. Inhibiting IRE1 enhances CD95-mediated cell death in glioblastoma and triple-negative breast cancer.

Keywords:
CD95Cell DeathER StressIRE1Unfolded Protein Response

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Area of Science:

  • Cancer Biology
  • Molecular Cell Biology
  • Signaling Pathways

Background:

  • Unfolded Protein Response (UPR) and Death Receptor (DR) signaling are often co-opted for tumor progression.
  • IRE1 is a key sensor of the UPR, implicated in cancer cell survival and proliferation.

Purpose of the Study:

  • To investigate the regulatory role of IRE1 in controlling Death Receptor CD95/Fas expression and function.
  • To explore the therapeutic potential of targeting the IRE1-CD95 axis in glioblastoma and triple-negative breast cancer.

Main Methods:

  • Genetic and pharmacologic inhibition of IRE1 activity.
  • Analysis of CD95 mRNA expression and its regulation by Regulated IRE1-Dependent Decay of RNA (RIDD).
  • Assessment of CD95L-induced cell death in cancer cell lines and in vivo mouse models.

Main Results:

  • IRE1 inhibition increased CD95 expression and sensitized glioblastoma and triple-negative breast cancer cells to CD95L-induced death.
  • CD95 mRNA is a target of IRE1-mediated RIDD.
  • IRE1 inhibition reduced CD95-mediated hepatic toxicity in mice.
  • XBP1s overexpression increased CD95 expression and cell death sensitivity.

Conclusions:

  • IRE1 exerts dual control over CD95-dependent cell death via RIDD and XBP1s.
  • This study reveals a novel regulatory link between IRE1 and CD95 signaling in cancer.
  • Targeting IRE1 may offer a therapeutic strategy to enhance CD95-mediated anti-tumor immunity.