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Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
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p53 and miR-210 regulated NeuroD2, a neuronal basic helix-loop-helix transcription factor, is downregulated in

Rahul Agrawal1, Ankita Garg1, Prit Benny Malgulwar2

  • 1Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology Delhi, New Delhi, India.

International Journal of Cancer
|December 12, 2017
PubMed

Insights

Neurogenic differentiation factor NeuroD2 is downregulated in glioblastoma (GBM), correlating with poor survival. Its overexpression suppresses GBM aggressiveness, suggesting a potential therapeutic strategy.

Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Molecular Oncology

Background:

  • Cell differentiation factors are implicated in tumor pathogenesis but their role in glioblastoma (GBM) is unclear.
  • Glioblastoma (GBM) is an aggressive brain tumor with limited therapeutic options.

Purpose of the Study:

  • To investigate the role of neurogenic differentiation factor NeuroD2 in glioblastoma (GBM).
  • To explore NeuroD2 as a potential prognostic biomarker and therapeutic target in GBM.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) GBM data and a patient cohort.
  • Investigation of NeuroD2 regulation by p53 and miR-210.
  • Assessment of NeuroD2's effect on GBM cell proliferation, migration, apoptosis, and 3D spheroid formation under hypoxia.

Main Results:

  • NeuroD2 is significantly downregulated in GBM, correlating with reduced patient survival.
  • NeuroD2 is induced by p53 and targeted by miR-210.
  • NeuroD2 overexpression inhibits GBM cell proliferation, migration, and 3D growth, while promoting apoptosis, particularly under hypoxia.
  • Enrichment analysis revealed NeuroD2 gene signature in pathways like cytokine-cytokine receptor interaction and PI3K-AKT signaling.

Conclusions:

  • NeuroD2 acts as a tumor suppressor and prognostic biomarker in GBM.
  • NeuroD2 levels are regulated by p53 and miR-210.
  • Overexpressing NeuroD2 presents a potential therapeutic strategy against GBM.
Keywords:
NeuroD2glioblastomahypoxiamiR-210p53

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