Vanadium induces AP-1- and NFκB-dependent transcription activity

Chuanshu Huang, Nanyue Chen, Wei-Ya Ma, Zigang Dong

Research output: Contribution to journalArticlepeer-review

48 Scopus citations

Abstract

Vanadate has been reported to be involved in the causation of cancer. In this study, we found that both AP-1 and NFκB activities were increased after treatment with sodium vanadate in JB6 cells. Maximum induction of AP-1 and NFκB appeared at 48 to 72 h. Phosphorylations of Erks and p38 kinases were markedly increased at 100 μM of vanadate, while phosphorylation of JNKs was not affected. Vanadate also enhances the phosphorylation of IκBα. These results suggest that the activation of AP-1 and NFκB by vanadate may be mediated through enhancement of phosphorylation of Erk/p38 kinases and IκBα, respectively.

Original languageEnglish (US)
Pages (from-to)711-715
Number of pages5
JournalInternational Journal of Oncology
Volume13
Issue number4
StatePublished - Oct 1998

Keywords

  • AP-1
  • NFκB
  • Vanadium

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