Related Experiment Video

Updated: Oct 19, 2025

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma
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SON drives oncogenic RNA splicing in glioblastoma by regulating PTBP1/PTBP2 switching and RBFOX2 activity

Jung-Hyun Kim1,2, Kyuho Jeong2, Jianfeng Li1,3

  • 1Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.

Nature Communications
|September 22, 2021
PubMed

Insights

SON is a master regulator of RNA splicing in glioblastoma multiforme (GBM). Its knockdown inhibits GBM cell growth by suppressing oncogenic splicing, making SON a potential therapeutic target for brain tumors.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Neuro-Oncology

Background:

  • RNA splicing dysregulation is an emerging cancer therapy target.
  • The role of splicing factors in brain tumors, particularly glioblastoma multiforme (GBM), remains unclear.

Purpose of the Study:

  • To investigate the role of RNA splicing factor SON in glioblastoma multiforme (GBM).
  • To elucidate the mechanism by which SON influences oncogenic and neuronal splicing pathways in GBM.
  • To evaluate SON as a potential therapeutic target for GBM.

Main Methods:

  • Identification of SON as a master regulator in GBM.
  • Analysis of SON's interaction with PTBP1 and RBFOX2 splicing factors.
  • Assessment of SON knockdown effects on GBM cell proliferation, clonogenicity, and tumor growth in vivo.

Main Results:

  • SON is overexpressed in GBM and acts as a master regulator of RNA splicing.
  • SON knockdown leads to PTBP1 downregulation and inhibition of oncogenic splicing.
  • SON antagonizes RBFOX2, suppressing neuronal splicing events.
  • SON inhibition reduces GBM cell proliferation, clonogenicity, and tumor growth.

Conclusions:

  • SON-mediated RNA splicing represents a vulnerability in GBM.
  • SON is implicated as a potential therapeutic target for brain tumors, specifically GBM.

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