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DRR1 promotes glioblastoma cell invasion and epithelial-mesenchymal transition via regulating AKT activation

Yu-Shui Ma1, Zhi-Jun Wu2, Rui-Zhen Bai3

  • 1Shanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, College of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200062, China.

Cancer Letters
|March 18, 2018
PubMed

Insights

High expression of DRR1 correlates with poor survival in glioblastoma (GBM). DRR1 depletion inhibits GBM invasion by regulating epithelial-mesenchymal transition (EMT) and AKT signaling.

Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Molecular Mechanisms

Background:

  • Metastatic invasion is a key factor in glioblastoma (GBM) treatment failure.
  • Epithelial-mesenchymal transition (EMT) is critical for GBM invasion.
  • Understanding EMT's molecular drivers is vital for developing new GBM therapies.

Purpose of the Study:

  • To investigate the role of DRR1 in GBM invasion and progression.
  • To elucidate the molecular mechanisms underlying DRR1's function in GBM.

Main Methods:

  • Correlative analysis of DRR1 expression with patient survival data.
  • Loss-of-function assays using short hairpin RNA (shRNA) targeting DRR1 (shDRR1) in GBM cell lines.
  • Assessment of EMT markers and AKT pathway activation (p-AKT).
  • Pharmacological inhibition of AKT signaling using MK-2206.

Main Results:

  • High DRR1 expression was associated with shorter overall and relapse-free survival in GBM patients.
  • DRR1 depletion using shDRR1 reduced GBM cell line invasiveness by modulating EMT markers.
  • DRR1 depletion led to decreased p-AKT levels in GBM cells.
  • Inhibition of AKT signaling with MK-2206 suppressed invasion and altered EMT marker expression (Vimentin, N-cadherin, MMP-7, snail, slug, E-cadherin).

Conclusions:

  • DRR1 plays a significant role in GBM invasion and progression.
  • DRR1 may promote EMT activation through the phosphorylation of AKT.
  • Targeting DRR1 or the AKT pathway presents a potential therapeutic strategy for GBM.
Keywords:
AKTDRR1EMTGBMInvasion

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