Vanadium induces AP-1- and NFkappB-dependent transcription activity.

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