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DDX3X mutation and Epstein-Barr virus cooperate to induce R-loop-dependent oncogenesis.

Hua-Man Cai1, Yu-Ran Qiu1, Yun Tan1

  • 1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cell Reports
|September 6, 2025
PubMed
Summary

Mutations in RNA helicase DDX3X impair innate immunity and promote cancer by enabling Epstein-Barr virus (EBV) lytic gene BNLF2b. This leads to R-loop accumulation and genomic instability, offering new therapeutic targets.

Keywords:
CP: CancerCP: GenomicsDDX3XDNA damageEpstein-Barr virusR-loopsgenomic instabilityoncogenesissynthetic lethality

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • RNA helicase DDX3X is involved in inflammasome activation and antiviral responses.
  • Scattered DDX3X mutations are observed in lymphoid cancers.
  • Epstein-Barr virus (EBV) plays a role in oncogenesis.

Purpose of the Study:

  • To characterize common features of DDX3X mutations in lymphoid cancers.
  • To elucidate the role of DDX3X mutations in EBV-driven oncogenesis.
  • To investigate the functional interaction between DDX3X mutations and EBV.

Main Methods:

  • Molecular dynamics simulation and crystallization were used to study DDX3X mutations.
  • Conditional knockin transgenic mice (Ddx3x^449_450ET>DP) were utilized.
  • The effects of etoposide on DDX3X mutant tumors were examined.

Main Results:

  • DDX3X mutations impair STING/IRF-7/IFN-α/β-mediated innate immunity.
  • Mutations lead to overexpression of EBV lytic gene BNLF2b and increased R-loop formation.
  • BNLF2b expression in mice induces R-loop accumulation, genomic instability, and abnormal immune cell proliferation, promoting malignancy.
  • Etoposide treatment triggers synthetic lethality in DDX3X mutant BNLF2b positive tumors.

Conclusions:

  • DDX3X mutations interact with EBV to drive R-loop-dependent oncogenesis.
  • Findings illuminate EBV's pathogenic mechanism and suggest R-loop targeting therapies.
  • This research provides insights into diseases involving RNA helicase alterations.