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

✍ Scribed by Qing-Bai She; Chuanshu Huang; Yiguo Zhang; Zigang Dong

Publisher
John Wiley and Sons
Year
2002
Tongue
English
Weight
134 KB
Volume
33
Category
Article
ISSN
0899-1987

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✦ Synopsis

Abstract

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 NH~2~‐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. © 2002 Wiley‐Liss, Inc.

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