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Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes

C Fimognari1, M Nüsse, F Berti

  • 1Department of Pharmacology, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy.

Cellular and Molecular Life Sciences : CMLS
|January 18, 2003
PubMed

Insights

Sulforaphane affects normal and cancerous T cells. This study shows sulforaphane impacts cell growth and survival in lymphocytes, raising questions about its use in cancer prevention.

Area of Science:

  • Cell Biology
  • Immunology
  • Cancer Research

Background:

  • Sulforaphane shows potential chemopreventive effects.
  • Previous studies indicated sulforaphane induces cell cycle arrest and apoptosis in leukemia cells.
  • The specificity of sulforaphane's effects on neoplastic versus normal cells remains unclear.

Purpose of the Study:

  • To investigate the effects of sulforaphane on non-transformed human lymphocytes.
  • To determine if sulforaphane's chemopreventive effects are specific to neoplastic cells.

Main Methods:

  • Treatment of phytohemagglutinin-stimulated human lymphocytes with sulforaphane.
  • Analysis of cell cycle progression using flow cytometry.
  • Assessment of apoptosis and necrosis.
  • Evaluation of protein expression, including cyclin D3 and p53.

Main Results:

  • Sulforaphane induced cell cycle arrest at the G1 phase in normal human lymphocytes.
  • A decrease in cyclin D3 protein expression was observed.
  • Sulforaphane induced apoptosis and necrosis.
  • Increased p53 protein expression was noted, mediating apoptosis.

Conclusions:

  • Sulforaphane acts as a growth modulator for T cells, affecting both normal and transformed lymphocytes.
  • The cytotoxic effects of sulforaphane on normal lymphocytes raise concerns about its suitability for cancer chemoprevention.
  • Further research is needed to clarify the therapeutic window and safety profile of sulforaphane.

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