The paradox of arsenic: Molecular mechanisms of cell transformation and chemotherapeutic effects

Ann M. Bode, Zigang Dong

Research output: Contribution to journalReview articlepeer-review

222 Scopus citations

Abstract

Arsenic is a well-documented carcinogen that also appears to be a valuable therapeutic tool in cancer treatment. This creates a paradox for which no unified hypothesis has been reached regarding the molecular mechanisms that determine whether arsenic will act as a carcinogen or as an effectual chemotherapeutic agent. Much of our knowledge with respect to the actions of arsenic has been drawn from epidemiological or clinical studies. The actions of arsenic are likely to be related to cell type, arsenic species, and length and dose of exposure. Arsenic unquestionably induces apoptosis and may specifically target certain tumor cells. Research data strongly suggest that arsenic influences distinct signaling pathways involved in mediating proliferation or apoptosis, including mitogen-activated protein kinases, p53, activator protein-1 or nuclear factor kappa B. The primary purpose of this review is to examine recent findings, from this laboratory and others, that focus on the molecular mechanisms of arsenic's actions in cell transformation and as a therapeutic agent.

Original languageEnglish (US)
Pages (from-to)5-24
Number of pages20
JournalCritical Reviews in Oncology/Hematology
Volume42
Issue number1
DOIs
StatePublished - 2002

Keywords

  • Activator protein-1
  • Apoptosis
  • Cancer
  • JB6 epidermal cells
  • Mitogen-activated protein kinase
  • Nuclear factor kappa B
  • Tumor

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