N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-gamma sensitivity for apoptosis in human glioblastoma cells

Cancer Lett. 2008 Mar 8;261(1):26-36. doi: 10.1016/j.canlet.2007.11.016.

Abstract

Glioblastoma is the most malignant and prevalent brain tumor in humans. It is composed of heterogenic abnormal astroglial cells that avoid differentiation, maintain proliferation, and hardly commit apoptosis. N-(4-Hydroxyphenyl)retinamide (4-HPR) induced astrocytic differentiation and increased sensitivity to interferon-gamma (IFN-gamma) for apoptosis in human glioblastoma A172, LN18, and SNB19 cells. Combination of 4-HPR and IFN-gamma significantly inhibited human telomerase reverse transcriptase (hTERT), cyclin dependent kinase 2 (CDK2), and survivin to up-regulate caspase-8, caspase-9, and caspase-3 for increasing apoptosis in all glioblastoma cell lines. Hence, combination of 4-HPR and IFN-gamma should be considered for controlling growth of different human glioblastoma cells.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Apoptosis / drug effects*
  • Caspases / metabolism
  • Cell Cycle / drug effects*
  • Cell Differentiation / drug effects*
  • Fenretinide / pharmacology*
  • Glioblastoma / pathology*
  • Humans
  • Interferon-gamma / pharmacology*
  • Models, Biological
  • Telomerase / metabolism*
  • Tumor Cells, Cultured

Substances

  • Fenretinide
  • Interferon-gamma
  • Telomerase
  • Caspases