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GSK3 acts as a switch for transcriptional programs in a model of low-grade gliomagenesis.

Marilin S Koch1,2, Minh Deo1,2, Lena-Marie Schmitt1,2

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|April 30, 2025
PubMed
Summary

Mutations in isocitrate dehydrogenase (IDH)1/2 drive glioma development. Targeting WNT/GSK3 signaling profoundly altered cell fate, impacting proliferation and cellular architecture, suggesting GSK3

Keywords:
GSK3GliomaIDH mutationIDHmut-gliomagenesisWNT

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Isocitrate dehydrogenase (IDH)1/2 mutations are key drivers in low-grade glioma (LGG) development.
  • Malignant transformation in LGG requires additional genetic events beyond IDH mutations.
  • Signaling pathways crucial for LGG malignancy acquisition remain incompletely understood.

Purpose of the Study:

  • To identify critical events preceding IDH-mutant tumorigenesis.
  • To investigate the role of WNT/GSK3, TGF-β, and NOTCH signaling in early gliomagenesis.
  • To explore the functional, transcriptional, and translational impacts of pathway modulation.

Main Methods:

  • Utilized an in vitro model system for IDH1R132H-dependent gliomagenesis.
  • Employed chemical compounds to modulate WNT/GSK3, TGF-β, and NOTCH signaling pathways.
  • Assessed impacts on gene expression, protein levels, cell morphology, migration, and proliferation.

Main Results:

  • Perturbation of all targeted pathways affected the LGG marker L1CAM.
  • Modulation of WNT/GSK3 signaling induced significant molecular transformation, altering glioma-associated genes and cellular programs.
  • WNT/GSK3 pathway disruption led to altered cell morphology, increased migration, and enhanced proliferation, with RUNX2 identified as a key downstream effector.

Conclusions:

  • Disrupted WNT/GSK3 signaling fundamentally impacts cell fate in early low-grade gliomagenesis.
  • GSK3 inhibition abrogated cell proliferation, highlighting its central role.
  • GSK3 signaling warrants further investigation as a potential therapeutic target in LGG.