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Possible involvement of rapamycin-sensitive pathway in Bcl-2 expression in human neuroblastoma SH-SY5Y cells

Y Kitamura1, T Kosaka, S Shimohama

  • 1Department of Neurobiology, Kyoto Pharmaceutical University, Japan.

Japanese Journal of Pharmacology
|December 31, 1997
PubMed

Insights

Immunosuppressants like rapamycin enhance Bcl-2 protein in neuroblastoma cells. This suggests a signaling pathway involving tyrosine kinase, PI3K, and p70 S6K regulates Bcl-2 expression.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Bcl-2 protein is crucial for cell survival.
  • Understanding Bcl-2 regulation is vital for neuroblastoma research.

Purpose of the Study:

  • To investigate the regulation of Bcl-2 protein expression in human neuroblastoma SH-SY5Y cells.
  • To identify signaling pathways influencing Bcl-2 levels.

Main Methods:

  • Treatment of SH-SY5Y cells with various compounds: immunosuppressants (FK506, cyclosporin A, rapamycin), herbimycin A, wortmannin, and platelet-derived growth factor.
  • Analysis of 27-kDa Bcl-2alpha protein levels.

Main Results:

  • Immunosuppressants, particularly rapamycin, significantly enhanced Bcl-2alpha protein levels.
  • Herbimycin A and wortmannin also increased Bcl-2 expression.
  • Platelet-derived growth factor decreased Bcl-2 levels.

Conclusions:

  • Bcl-2 expression in neuroblastoma cells is modulated by specific signaling pathways.
  • The cascade involving tyrosine kinase, phosphatidylinositol 3-kinase, and rapamycin-sensitive p70 S6-kinase likely regulates Bcl-2.

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