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Updated: Feb 17, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
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Alu-dependent RNA editing of GLI1 promotes malignant regeneration in multiple myeloma

Elisa Lazzari1, Phoebe K Mondala1, Nathaniel Delos Santos1

  • 1Division of Regenerative Medicine, Department of Medicine, Moores Cancer Center, University of California, San Diego, La Jolla, CA, 92037, USA.

Nature Communications
|December 6, 2017
PubMed

Insights

Amplification of the ADAR1 gene promotes multiple myeloma (MM) progression and resistance to treatment. Inhibiting ADAR1 may prevent MM relapse and disease advancement.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Multiple myeloma (MM) frequently relapses despite new treatments.
  • Chromosome 1q amplification, including the ADAR1 gene, is common in MM and linked to poor outcomes.
  • RNA editing by adenosine deaminase acting on RNA (ADAR)1 is implicated in cancer progression.

Purpose of the Study:

  • To investigate the role of ADAR1 in MM progression and therapeutic resistance.
  • To determine the correlation between ADAR1 expression and patient survival.
  • To assess the impact of ADAR1 inhibition on MM regeneration.

Main Methods:

  • Analysis of ADAR1 RNA expression in the MMRF CoMMpass data set.
  • In vitro experiments assessing the effect of wild-type and mutant ADAR1 on GLI1 activity and drug resistance.
  • In vivo studies using patient-derived xenografts to evaluate ADAR1 knockdown effects on MM regeneration.

Main Results:

  • High ADAR1 RNA expression significantly correlates with reduced survival in MM patients.
  • Wild-type ADAR1 enhances GLI1 transcription and promotes resistance to immunomodulatory drugs.
  • ADAR1 knockdown reduces the regeneration of high-risk MM in xenograft models.

Conclusions:

  • ADAR1 promotes MM malignant regeneration and therapeutic resistance.
  • Targeting ADAR1 may offer a novel strategy to prevent MM progression and relapse.

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