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Transforming growth factor beta receptor family ligands inhibit hepatocyte growth factor synthesis and secretion from

Naibedya Chattopadhyay1, Jacob T-Felt Hansen, Madan M Godbole

  • 1Division of Endocrinology, Diabetes and Hypertension and Membrane Biology Program, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Rm 205, Boston, MA 02115, USA. Naibedya@rics.bwh.harvard.edu

Brain Research. Molecular Brain Research
|February 19, 2004
PubMed

Insights

Transforming growth factor beta (TGFbeta) and hepatocyte growth factor (HGF) influence glioma. Activin-A inhibits HGF secretion, suggesting its potential in combination glioma therapy.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Glioma progression is influenced by growth factors like TGFbeta and HGF.
  • U87 human astrocytoma cells express TGFbeta receptors (TbetaRs).

Purpose of the Study:

  • To investigate the effects of TGFbeta1, HGF, activin-A, and BMP-2 on U87 cell proliferation and HGF secretion.
  • To evaluate the potential of targeting TGFbeta receptor signaling for glioma therapy.

Main Methods:

  • Analysis of mRNA expression for Smads and relevant receptors in U87 cells.
  • Cell proliferation assays under different growth factor treatments.
  • Measurement of HGF secretion levels after TGFbeta1, activin-A, and BMP-2 treatments.

Main Results:

  • TGFbeta1 inhibited proliferation, while HGF induced it.
  • TGFbeta1 and activin-A significantly inhibited HGF secretion, more so than BMP-2.
  • None of the tested factors altered c-Met expression.

Conclusions:

  • Activin-A demonstrates potent inhibition of HGF secretion, making it a promising candidate for combination glioma therapy.
  • Interfering with TbetaR signaling requires careful consideration to avoid negating beneficial HGF inhibition.

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