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Protein kinase C regulates bombesin-induced rapid VEGF secretion in neuroblastoma cells

Cameron Schlegel1, Pritha Paul, Sora Lee

  • 1Department of Pediatric Surgery, 2200 Children's Way, DOT 7100, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Anticancer Research
|November 17, 2012
PubMed
Abstract

Insights

Protein kinase C (PKC) drives rapid vascular endothelial growth factor (VEGF) secretion via gastrin-releasing peptide (GRP) receptor signaling in neuroblastoma cells, impacting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Gastrin-releasing peptide (GRP) receptor signaling in neovascularization remains unclear.
  • Investigating the cellular mechanisms of GRP receptor regulation of vascular endothelial growth factor (VEGF) in neuroblastoma.

Purpose of the Study:

  • To elucidate the intracellular signaling pathways mediating GRP receptor-induced VEGF release.
  • To determine the role of protein kinase C (PKC) in this process.

Main Methods:

  • BE(2)-C neuroblastoma cells were treated with bombesin (BBS), a PKC agonist (PMA), or a PKC inhibitor (GFX).
  • VEGF secretion, and phosphorylation of AKT, ERK, and PKD were analyzed.
  • Immunofluorescent staining for VEGF was performed.

Main Results:

  • Bombesin (BBS) significantly increased VEGF secretion within 30 minutes.
  • PMA treatment alone elevated VEGF secretion, synergistically enhanced by GRP.
  • GFX inhibited PMA-stimulated VEGF secretion, indicating PKC's role.

Conclusions:

  • Protein kinase C (PKC) is essential for rapid VEGF secretion mediated by GRP receptor signaling in neuroblastoma.
  • VEGF inhibition markedly reduced GRP-induced cell proliferation, highlighting its importance in neuroblastoma tumorigenesis.

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