Sulforaphane prevents mouse skin tumorigenesis during the stage of promotion

Joell J Gills1, Elizabeth H Jeffery, Nathan V Matusheski

  • 1Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL 60612, USA.

Cancer Letters
|July 5, 2005
PubMed

Insights

Sulforaphane (SF), a natural compound from broccoli, effectively inhibited skin tumor development in mice when applied after carcinogen exposure. SF also reduced a key enzyme activity linked to tumor promotion.

Area of Science:

  • Chemoprevention
  • Natural Products
  • Cancer Research

Background:

  • Sulforaphane (SF) is a natural compound found in broccoli with known anti-carcinogenic properties.
  • Previous studies suggest SF inhibits tumor growth, cell cycle progression, and induces apoptosis.
  • SF's role in blocking chemical carcinogenesis initiation and promotion has been investigated.

Purpose of the Study:

  • To evaluate the efficacy of topical Sulforaphane (SF) in preventing mouse skin tumorigenesis.
  • To investigate the effect of SF on specific molecular mechanisms involved in carcinogenesis, such as ornithine decarboxylase activity.

Main Methods:

  • Topical application of SF (1, 5, or 10 micromol/mouse) in mouse skin tumorigenesis models induced by 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol 13-acetate (TPA).
  • SF was administered using anti-promotion and combined anti-initiation/anti-promotion protocols.
  • Measurement of TPA-induced ornithine decarboxylase activity in mouse skin.

Main Results:

  • Topical SF significantly inhibited TPA-induced mouse skin tumorigenesis under anti-promotion and combined protocols.
  • SF did not show a significant effect when applied solely as an anti-initiation treatment.
  • SF administration inhibited TPA-induced ornithine decarboxylase activity in mouse skin.

Conclusions:

  • Sulforaphane demonstrates significant chemopreventive effects against mouse skin tumorigenesis, particularly when applied during the promotion phase.
  • The inhibition of ornithine decarboxylase activity by SF is a key molecular mechanism underlying its anti-promotion effects.
  • SF's efficacy is dependent on the timing of application relative to carcinogen exposure.