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RIPK3 promotes adenovirus type 5 activity.

Melanie Weigert1, Alex Binks1, Suzanne Dowson1

  • 1Institute of Cancer Sciences, University of Glasgow, Garscube Estate, Glasgow, G61 1QH, UK.

Cell Death & Disease
|December 15, 2017
PubMed
Summary
This summary is machine-generated.

Oncolytic adenoviruses cause cancer cell death, but the mechanism is unclear. This study reveals adenovirus-induced cell death differs from classical necroptosis, involving RIPK3 but not MLKL, offering new therapeutic insights.

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Area of Science:

  • Oncolytic virotherapy
  • Cell death mechanisms
  • Immunology

Background:

  • Oncolytic adenoviruses selectively infect and kill cancer cells, potentially activating immune responses.
  • The precise mechanism of adenovirus-induced cell death, particularly its resemblance to necroptosis, remains incompletely understood.

Purpose of the Study:

  • To investigate the roles of key necrosis proteins (RIPK1, RIPK3, MLKL) in adenovirus-mediated cytotoxicity.
  • To elucidate the mechanism of cell death induced by the oncolytic adenovirus mutant dl922-947 and compare it to TNF-α-induced necroptosis (TSZ).

Main Methods:

  • Electron microscopy to analyze cell morphology.
  • CRISPR/Cas9 gene editing to assess the roles of RIPK1, RIPK3, and MLKL.
  • In vitro and in vivo efficacy studies of adenovirus mutants.

Main Results:

  • Adenovirus dl922-947 induced necrotic morphology similar to TSZ but was independent of TNF-α signaling and RIPK1.
  • Adenovirus-induced cell death did not require MLKL, distinguishing it from classical necroptosis.
  • Caspase-8 inhibition enhanced dl922-947 cytotoxicity in a RIPK3- and MLKL-dependent manner.
  • RIPK3 expression promoted adenovirus efficacy independently of caspase inhibition.

Conclusions:

  • Adenovirus-induced programmed necrosis is mechanistically distinct from classical necroptosis.
  • RIPK3 plays a crucial role in enhancing adenovirus oncolytic efficacy, even without caspase inhibition.
  • Understanding these distinct cell death pathways can inform the development of more effective oncolytic virotherapies.