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Effect of Ras-guanine nucleotide release factor 1-mediated H-Ras/ERK signaling pathway on glioma

Yi-Heng Pan1, Jing Chen1, Cui Sun1

  • 1Center for Diagnosis and Treatment of Neuro-oncology Diseases, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei, China.

Brain Research
|January 7, 2021
PubMed
Abstract

Insights

Ras-guanine nucleotide release factor 1 (Ras-GRF1) is upregulated in glioma and promotes tumor growth and metastasis by activating the H-Ras/ERK pathway. Silencing Ras-GRF1 may suppress glioma progression.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Glioma is a primary brain tumor with poor prognosis.
  • The Ras-guanine nucleotide release factor 1 (Ras-GRF1) role in glioma remains unclear.
  • Understanding signaling pathways involved in glioma is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the function of Ras-guanine nucleotide release factor 1 (Ras-GRF1) in glioma.
  • To elucidate the role of Ras-GRF1 in mediating the H-Ras/ERK signaling pathway in glioma.
  • To explore Ras-GRF1 as a potential therapeutic target for glioma.

Main Methods:

  • Immunohistochemistry was used to detect Ras-GRF1, H-Ras, K-Ras, and N-Ras expression in glioma and normal brain tissues.
  • Glioma cells were transfected with Ras-GRF1 siRNA, H-Ras siRNA, and Ras-GRF1 lentivirus.
  • Cell proliferation, clonogenic ability, migration, invasion, and apoptosis were evaluated using MTT, plate clone formation, wound-healing, Transwell, and Annexin-V/PI assays, respectively.
  • Western blotting measured protein expression, and in vivo studies utilized subcutaneous and orthotopic mouse models.

Main Results:

  • Ras-GRF1, H-Ras, K-Ras, and N-Ras expressions were upregulated in glioma tissues and correlated with WHO grade.
  • Ras-GRF1 expression positively correlated with H-Ras expression.
  • Ras-GRF1 silencing reduced H-Ras and p-ERK/ERK expression, inhibiting glioma cell proliferation, clone formation, migration, and invasion while enhancing apoptosis.
  • In vivo, Ras-GRF1 silencing reduced tumor volume and weight, with decreased H-Ras and p-ERK/ERK levels.

Conclusions:

  • Ras-GRF1 is upregulated in glioma, correlating with malignancy and prognosis.
  • Ras-GRF1 promotes glioma growth and metastasis by mediating the H-Ras/ERK pathway.
  • Targeting Ras-GRF1 may represent a novel therapeutic strategy for glioma.
Keywords:
GliomaH-Ras/ERKRas-GRF1

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