Involvement of Erks activation in cadmium-induced AP-1 transactivation in vitro and in vivo

C. Huang, Q. Zhang, J. Li, X. Shi, V. Castranova, G. Ju, M. Costa, Z. Dong

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Cadmium is a potent and effective carcinogen in rodents and has recently been accepted by IARC (International Agency for Research on Cancer) as a category 1 carcinogen. Cadmium-induced up-regulation of intracellular signaling pathways leading to increased mitogenesis is thought to be a major mechanism for the carcinogenic activity following chronic cadmium exposure. In the present study, we found that exposure of cells to cadmium induced significant activation of AP-1 and all three members of the MAP kinase family in mouse epidermal JB6 cells. The induction of AP-1 activity by cadmium appears to involve activation of Erks, since the induction of AP-1 activity by cadmium was blocked by pretreatment of cells with PD98058. Interestingly, the induction of AP-1 by cadmium was greatly enhanced by the chemical tumor promoter, TPA and the growth factor EGF, but not by ultraviolet C radiation. In vivo studies demonstrated that cadmium could also induce transactivation of AP-1 in AP-1-luciferase report transgenic mice. Considering the role of AP-1 activation in tumor promotion, the results presented in this study provide a possible molecular mechanism for cadmium-induced carcinogenesis.

Original languageEnglish
Pages (from-to)141-147
Number of pages7
JournalMolecular and Cellular Biochemistry
Issue number1-2
StatePublished - 2001

Bibliographical note

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


  • AP-1
  • Cadmium
  • Transgenic and MAP kinase

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology


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