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Fas/Fas ligand regulation mediates cell death in human Ewing's sarcoma cells treated with melatonin

G García-Santos1, V Martin, J Rodríguez-Blanco

  • 1Departamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, C/ Julian Claveria 6, 33006 Oviedo, Spain.

British Journal of Cancer
|March 3, 2012
PubMed
Abstract

Insights

Melatonin induces cell death in Ewing's sarcoma by increasing Fas and Fas Ligand (Fas L) expression. This molecule also transiently increases oxidants and activates Nuclear Factor-kappaB, crucial for its cytotoxic effect in these cancer cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ewing's sarcoma has a poor prognosis, necessitating novel therapeutic strategies.
  • Melatonin has demonstrated prior ability to induce apoptosis in Ewing's sarcoma cells via the extrinsic pathway.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying melatonin-induced apoptosis in Ewing's sarcoma.
  • To investigate the role of oxidative stress and transcription factor activation in melatonin's cytotoxic effects.

Main Methods:

  • Cell viability assays
  • Flow cytometry
  • Quantitative PCR
  • Western blotting
  • Electrophoretic mobility shift assay

Main Results:

  • Melatonin upregulates Fas and Fas Ligand (Fas L) expression, mediating cell death.
  • Melatonin induces a transient increase in intracellular oxidants and activates Nuclear Factor-kappaB (NF-κB).
  • Inhibition of NF-κB activation abrogates melatonin-induced cell death and Fas/Fas L upregulation.

Conclusions:

  • Melatonin's cytotoxic effect in Ewing's sarcoma is mediated by the Fas/Fas L pathway and NF-κB activation.
  • Differences in cellular biology may explain melatonin's selective toxicity in certain cancer types.
  • Melatonin represents a potential therapeutic agent for Ewing's sarcoma, warranting further investigation.

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