Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

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

Authors
Huang-C; Zhang-Q; Li-J; Shi-X; Castranova-V; Ju-G; Costa-M; Dong-Z
Source
Mol Cell Biochem 2001 Jun; 222(1-2):141-147
NIOSHTIC No.
20021757
Abstract
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 I 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.
Keywords
Cadmium-compounds; In-vitro-studies; In-vivo-studies; Carcinogens; Carcinogenesis; Carcinogenicity; Exposure-levels; Exposure-assessment; Growth-factors
Contact
Nelson Institute of Environmental Medicine, New York University School of Medicine, NY 10016
CODEN
MCBIB8
CAS No.
7440-43-9
Publication Date
20010601
Document Type
Journal Article
Fiscal Year
2001
NTIS Accession No.
NTIS Price
Issue of Publication
1-2
ISSN
0300-8177
NIOSH Division
HELD
Source Name
Molecular and Cellular Biochemistry
State
WV; NY; MN
TOP