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Cyanidin-3-glucoside suppresses B[a]PDE-induced cyclooxygenase-2 expression by directly inhibiting Fyn kinase

Tae-Gyu Lim1, Jung Yeon Kwon, Jiyoung Kim

  • 1Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Seoul, Republic of Korea.

Biochemical Pharmacology
|April 20, 2011
PubMed

Insights

Cyanidin-3-glucoside (C3G) inhibits benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE)-induced cyclooxygenase-2 (COX-2) expression. C3G suppresses B[a]PDE-induced skin cancer by blocking the Fyn signaling pathway.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE) is a carcinogen linked to skin cancer.
  • Cyclooxygenase-2 (COX-2) expression is crucial in inflammation and tumor promotion.

Purpose of the Study:

  • To investigate the inhibitory effect of cyanidin-3-glucoside (C3G) on B[a]PDE-induced COX-2 expression.
  • To elucidate the molecular mechanisms underlying C3G's action in mouse epidermal cells.

Main Methods:

  • Treatment of mouse epidermal JB6 P+ cells with C3G and B[a]PDE.
  • Analysis of COX-2 expression, promoter activity, and signaling pathways (AP-1, NF-κB, MAPKs, Fyn).
  • Kinase assays and use of pharmacological inhibitors (PP2) to study Fyn kinase activity.

Main Results:

  • C3G pretreatment reduced B[a]PDE-induced COX-2 expression and promoter activity.
  • C3G attenuated the activation of AP-1, NF-κB, and phosphorylation of MEK, MKK4, Akt, and MAPKs.
  • C3G directly inhibited Fyn kinase activity, revealing Fyn's role in B[a]PDE-induced COX-2 expression.

Conclusions:

  • Cyanidin-3-glucoside suppresses B[a]PDE-induced COX-2 expression primarily by inhibiting the Fyn signaling pathway.
  • C3G demonstrates potential chemopreventive properties against skin cancer induced by B[a]PDE.

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