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MYCN and helicases DDX17 and DDX5 have opposite effects on the production of readthrough-associated chimeric

Valentine Clerc1, Khouaila Aouadi1, Jessica Valat1

  • 1Equipe Labellisée Ligue Contre Le Cancer, Laboratoire de Biologie Et Modelisation de La Cellule, Ecole Normale Superieure de Lyon, CNRS, UMR 5239, Inserm, U1293, Universite Claude Bernard Lyon 1, 69007, Lyon, France.

Cellular and Molecular Life Sciences : CMLS
|May 28, 2026
PubMed

Insights

DEAD box helicases DDX17 and DDX5 are crucial for RNA processing. Their depletion in neuroblastoma cells increases harmful chimeric RNAs (tracRNAs), linked to high-risk tumors and poor survival.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • RNA Biology

Background:

  • DEAD box helicases DDX17 and DDX5 regulate transcription termination and pre-messenger RNA 3' end processing.
  • Dysregulation of these helicases is implicated in various cellular processes.

Purpose of the Study:

  • To investigate the role of DDX17 and DDX5 in neuroblastoma.
  • To explore the impact of their depletion on RNA processing and tumor characteristics.
  • To elucidate the relationship between MYCN, DDX17/DDX5, and transcription termination.

Main Methods:

  • Depletion of DDX17 and DDX5 in neuroblastoma cell lines.
  • Analysis of transcriptomic data from neuroblastoma tumors.
  • Investigation of MYCN binding and interactions with DDX17.

Main Results:

  • DDX17 depletion induces transcriptional readthrough and increases chimeric RNAs (tracRNAs).
  • Low DDX17/DDX5 expression correlates with high-risk neuroblastoma, poor survival, and MYCN amplification.
  • MYCN directly binds gene 3' regions and interacts with DDX17, affecting transcription termination.

Conclusions:

  • MYCN plays a novel role in regulating transcription termination.
  • Deregulation of MYCN and DDX17/DDX5 promotes the expression of potentially harmful non-canonical RNA molecules in neuroblastoma.
  • This highlights a new mechanism contributing to neuroblastoma progression.

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