Epidemiological and animal studies suggest that several metals and metal-containing compounds are potent mutagens and carcinogens. These metals include chromium, arsenic, vanadium, nickel, and others. During the last two decades, chemical and cellular studies have contributed enormously to our understanding of the mechanisms of metal-induced pathophysiological processes. Although each of these metals is unique in its mechanism of action, some common signaling molecules, such as reactive oxygen species (ROS), may be shared by many of the carcinogenic metals. New techniques are now available to reveal the mechanisms of carcinogenesis in precise molecular terms. In this review, we focused our attentions on carcinogenic metal-induced signal transduction pathways leading to the activation of NF-κB, cell apoptosis and cell cycle progression, three crucial steps or events involved in the transformation and carcinogenesis. This review summarizes current knowledge and our recent studies concerning intracellular signal transduction pathways initiated by carcinogenic metals and the cross-talk that occurs among these pathways in cells in response to metals.
|Number of pages
|Critical Reviews in Oncology/Hematology
|Published - 2002
Bibliographical noteFunding Information:
We thank Dr Val Vallyathan, Dr Vince Castranova and Dr Murali Rao for helpful suggestions and critique of the manuscript. We apologize to all authors whose primary valuable work could not be cited, because of space constrains. F. Chen thanks the Health Effects Laboratory Division of National Institute for Occupational Safety and Health for support through a cooperative agreement from the Association of Teachers of Preventive Medicine and the Centers for Disease Control and Prevention of the United States.
Copyright 2008 Elsevier B.V., All rights reserved.
- Cell cycle
- Signal transduction
ASJC Scopus subject areas