Inhibition of AP-1 and neoplastic transformation by fresh apple peel extract

Min Ding1, Yongju Lu, Linda Bowman

  • 1Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA. mid5@cdc.gov

Insights

Apple peel extract reduced skin tumors in mice by scavenging free radicals. This extract also blocked key cell signaling pathways involved in tumor promotion, suggesting chemopreventive potential.

Area of Science:

  • Oncology
  • Dermatology
  • Biochemistry

Background:

  • Fruit and vegetable consumption is linked to reduced cancer risk.
  • Previous research indicates fresh apples may inhibit tumor cell proliferation.

Purpose of the Study:

  • To investigate the chemopreventive effects of apple peel extract on skin carcinogenesis.
  • To elucidate the mechanisms underlying the potential anti-cancer properties of apple peel extract.

Main Methods:

  • Oral administration of apple peel extract to mice initiated with 7,12-dimethylbenz(a)anthracene and promoted with 12-O-tetradecanolyphorbol-13-acetate (TPA).
  • Electron Spin Resonance (ESR) analysis to assess radical scavenging activity.
  • Mechanistic studies involving JB6 cells and AP-1-luciferase reporter transgenic mice to evaluate inhibition of AP-1 transactivation and MAPK signaling (ERK and JNK).

Main Results:

  • Apple peel extract significantly decreased the number of nonmalignant and malignant skin tumors per mouse.
  • The extract demonstrated potent scavenging of hydroxyl (OH) and superoxide (O(2)(-)) radicals.
  • Pretreatment with apple peel extract inhibited TPA- and ultraviolet B-induced AP-1 transactivation by blocking ERK and JNK activity.

Conclusions:

  • Fresh apple peel extract exhibits chemopreventive effects against tumor promoter-induced skin carcinogenesis in mice.
  • The observed chemopreventive effects are likely mediated by the extract's antioxidant properties, specifically by inhibiting reactive oxygen species-mediated AP-1 and MAPK pathway activation.

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