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B in malignant
melanoma cells
1 Departments of Internal Medicine and the Cannon Research Center, Carolinas Medical Center, Charlotte 28232; 2 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham 27710; 4 National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711; and 3 Division of Respiratory, Critical Care, and Occupational (Pulmonary) Medicine, University of Utah, Salt Lake City, Utah 84132
The transcription factor nuclear factor-
B (NF-B) is
constitutively activated in malignancies from enhanced activity of inhibitor of NF-B (IB) kinase, with accelerated IB
degradation. We studied whether redox signaling might stimulate these
events. Cultured melanoma cells generated superoxide anions
(O
) without serum stimulation. O
generation was reduced by the NAD(P)H:quinone oxidoreductase (NQO)
inhibitor dicumarol and the quinone analog capsaicin, suggesting that
electron transfer from NQO through a quinone-mediated pathway may be an important source of endogenous reactive oxygen species (ROS) in tumor
cells. Treatment of malignant melanoma cells with the
H2O2 scavenger catalase, the sulfhydryl donor
N-acetylcysteine, the glutathione peroxidase mimetic
ebselen, or dicumarol decreased NF-B activation. Catalase,
N-acetylcysteine, ebselen, dicumarol, and capsaicin also
inhibited growth of melanoma and other malignant cell lines. These
results raise the possibility that ROS produced endogenously by
mechanisms involving NQO can constitutively activate NF-B in an
autocrine fashion and suggest the potential for new antioxidant
strategies for interruption of oxidant signaling of melanoma cell growth.
nuclear factor-B; superoxide anion; hydrogen peroxide; tumor; neoplasm; dicumarol
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