Modulation of skin tumorigenesis by SOD

Daret St. Clair, Yunfeng Zhao, Luksana Chaiswing, Terry Oberley

Research output: Contribution to journalArticlepeer-review

48 Scopus citations

Abstract

Generation of reactive oxygen species (ROS) has been implicated in the development of cancer. Groundwork establishing mitochondria as a critical source of ROS generation and the role of manganese superoxide dismutase (MnSOD) in preventing mitochondria-mediated cell death have been well established. In a seemingly contradictory role, it also is well documented that increased MnSOD expression suppresses the carcinogenesis effect of ROS. Our recent studies demonstrated that overexpression of MnSOD reduced tumor incidence in the two-stage 7,12-dimethylbenz(a)-anthracene (DMBA)/12-O-tetradecanoylphorbol-13- acetate (TPA) skin carcinogenesis model. However, reduction of MnSOD by heterozygous knockout of the MnSOD gene (Sod 2+/-) did not lead to an increase in tumor incidence. Thus, how modulation of mitochondrial ROS levels alter the outcome of developing cancer is unclear. This review will provide background information on the sequence of ROS-mediated events in the mitochondria and evidence that suggests that the antioxidant and tumor suppressor functions of MnSOD are indeed inter-related. It also will offer insights into the mechanisms by which MnSOD modulates the outcome of early stage skin carcinogenesis.

Original languageEnglish
Pages (from-to)209-214
Number of pages6
JournalBiomedicine and Pharmacotherapy
Volume59
Issue number4
DOIs
StatePublished - May 2005

ASJC Scopus subject areas

  • Pharmacology

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