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Protein kinase C mediates induced secretion of vascular endothelial growth factor by human glioma cells

Jui-Chang Tsai1, Lee-Jene Teng, Chin-Tin Chen

  • 1Division of Neurosurgery, Department of Surgery, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei 100, Taiwan. jctsai@ha.mc.ntu.edu.tw

Biochemical and Biophysical Research Communications
|September 19, 2003
PubMed

Insights

Protein tyrosine kinase (PTK) and protein kinase C (PKC) pathways regulate vascular endothelial growth factor (VEGF) production in glioma cells. Inhibiting these kinases reduces glioma proliferation and VEGF secretion, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Malignant gliomas secrete vascular endothelial growth factor (VEGF), promoting tumor growth and angiogenesis.
  • Understanding the signaling pathways that control VEGF production is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the roles of protein tyrosine kinase (PTK) and protein kinase C (PKC) in regulating VEGF production in malignant glioma cells.
  • To determine the relationship between glioma cell proliferation and VEGF secretion.

Main Methods:

  • Utilized specific inhibitors of PTK and PKC (e.g., genistein, H-7) to block signaling pathways.
  • Stimulated VEGF secretion using growth factors (EGF, PDGF-BB, bFGF) and activators (PMA, A23187).
  • Monitored glioma cell proliferation and VEGF secretion levels in response to treatments.

Main Results:

  • PTK inhibitors blocked glioma proliferation and epidermal growth factor (EGF)-induced VEGF secretion.
  • PKC inhibition (H-7) reduced both baseline and EGF-induced VEGF secretion.
  • PKC activation (PMA) stimulated VEGF secretion, but this was blocked by prolonged PMA treatment, suggesting PKC depletion.
  • Inhibitors affecting VEGF secretion also inhibited cell proliferation at similar concentrations.
  • PKC inhibition accounted for only 50% of growth factor-induced VEGF secretion, indicating a PKC-independent component.

Conclusions:

  • VEGF production in glioma cells is tightly regulated by both PTK and PKC signaling pathways.
  • These pathways are closely linked to glioma cell proliferation.
  • Convergent growth factor signaling pathways activate VEGF secretion, suggesting multiple therapeutic targets.
  • Further understanding of these signaling mechanisms can inform novel anti-glioma strategies.

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