Rhein inhibits TPA-induced activator protein-1 activation and cell transformation by blocking the JNK-dependent pathway.

Shigang Lin, Jian-Jian Li, Makoto Fujii, De Xing Hou

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

Rhein (4,5-Dihydroxyanthraquinone-2-carboxylic acid), a constituent enriched in the rhizome of rhubarb (R. palmatum L. or R. tanguticum Maxim), is a traditional Chinese herb used as a laxative and stomachic drug. In the present study, we investigated the anti-carcinogenesis of rhein by using mouse epidermal cell JB6 line, an in vitro model for elucidating the molecular mechanisms of cancer chemopreventive agents. Rhein is shown to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell transformation and activator protein-1 (AP-1) activation in a dose-dependent manner. Signal cascade analysis revealed that rhein inhibits the phosphorylation and abundance of c-Jun protein, c-Jun NH2-terminal kinase (JNK) phosphorylation, but does not inhibit the phosphorylation of extracellular signal-regulated protein kinase (ERK) and p38 kinase. Thus, these results provide the first evidence suggesting that rhein inhibits AP-1 activity and cell transformation through the inhibition of a JNK-dependent, ERK- and p38-independent molecular mechanism.

Original languageEnglish (US)
Pages (from-to)829-833
Number of pages5
JournalInternational Journal of Oncology
Volume22
Issue number4
StatePublished - Apr 2003
Externally publishedYes

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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