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Autocrine control of human meningioma proliferation: secretion of platelet-derived growth-factor-like molecules

E F Adams1, T Todo, U M Schrell

  • 1Department of Neurosurgery, University of Erlangen-Nuremberg, Germany.

Insights

Human meningioma cells secrete platelet-derived growth factor (PDGF)-like molecules. These molecules stimulate meningioma cell proliferation, suggesting autocrine control in tumor growth.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Meningiomas are the most common primary tumors of the central nervous system.
  • The molecular mechanisms driving meningioma proliferation are not fully understood.

Purpose of the Study:

  • To investigate growth factor production by human meningioma cells.
  • To determine if meningioma cell proliferation is regulated by autocrine signaling.

Main Methods:

  • Cell-culture techniques were used to grow primary human meningioma cells.
  • Conditioned medium (MEN-CM) from meningioma cultures was used to stimulate IMR32 neuroblastoma cells and primary meningioma cells.
  • Neutralizing antibodies against platelet-derived growth factor (PDGF) and TGF-alpha were employed.
  • Size exclusion chromatography (Sephadex G-100) was used to characterize the molecular weight of mitogenic factors.

Main Results:

  • Conditioned medium from meningioma cells (MEN-CM) significantly stimulated the in vitro growth of both IMR32 and primary meningioma cells.
  • MEN-CM increased H3-thymidine uptake in cultured meningioma cells in a dose-dependent manner.
  • A neutralizing antibody against PDGF abolished the stimulatory effects of MEN-CM, while an antibody against TGF-alpha had no effect.
  • Mitogenic activity in MEN-CM eluted in three peaks corresponding to molecular weights >=150 kDa, 56 kDa, and 28 kDa.

Conclusions:

  • Human meningioma cells secrete PDGF-like molecules.
  • These secreted PDGF-like molecules stimulate meningioma cell proliferation.
  • Meningioma growth may be under autocrine control mediated by PDGF-like factors.

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