Involvement of c-jun NH2-terminal kinases in resveratrol-induced activation of p53 and apoptosis

Qing Bai She, Chuanshu Huang, Yiguo Zhang, Zigang Dong

Research output: Contribution to journalArticlepeer-review

100 Scopus citations


Resveratrol, a constituent of grapes and other foods, is one of the most promising agents for cancer prevention. In a previous study, we showed that the antitumor activity of resveratrol occurs through extracellular signal-regulated protein kinases (ERKs) and p38 kinase-mediated p53 activation. In this study, we also determined that c-jun NH2-terminal kinases (JNKs) are involved in resveratrol-induced p53 activation and induction of apoptosis. In the JB6 mouse epidermal cell line, resveratrol activated JNKs dose-dependently within a dose range of 10-40 μM, the same dosage responsible for the inhibition of tumor promoter-induced cell transformation. Stable expression of a dominant negative mutant of JNK1 or disruption of the Jnk1 or Jnk2 gene markedly inhibited resveratrol-induced p53-dependent transcription activity and induction of apoptosis. Furthermore, resveratrol-activated JNKs were shown to phosphorylate p53 in vitro, but this activity was repressed in the cells expressing a dominant negative mutant of JNK1 or in Jnk1 or Jnk2 knockout (Jnk1-/- or Jnk2-/-) cells. These data suggested that JNKs act as mediators of resveratrol-induced activation of p53 and apoptosis, which may occur partially through p53 phosphorylation.

Original languageEnglish
Pages (from-to)244-250
Number of pages7
JournalMolecular Carcinogenesis
Issue number4
StatePublished - 2002

Bibliographical note

Copyright 2008 Elsevier B.V., All rights reserved.


  • Apoptosis
  • C-jun NH-terminal kinases
  • P53
  • Resveratrol

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research


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