Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 98, Issue 10, Pages 5550-5555Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.101505898
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Funding
- NCI NIH HHS [R01 CA084138, CA84138] Funding Source: Medline
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Nox1, a homologue of gp91phox, the catalytic moiety of the superoxide (O-2(-))-generating NADPH oxidase of phagocytes, causes increased O-2(-) generation, increased mitotic rate, cell transformation, and tumorigenicity when expressed in NIH 3T3 fibroblasts. This study explores the role of reactive oxygen species (ROS) in regulating cell growth and transformation by Nox1. H2O2 concentration increased approximate to 10-fold in Nox1-expressing cells, compared with <2-fold increase in O-2(-). When human catalase was expressed in Nox1-expressing cells. H2O2 concentration decreased, and the cells reverted to a normal appearance, the growth rate normalized, and cells no longer produced tumors in athymic mice. A large number of genes, including many related to cell cycle, growth, and cancer (but unrelated to oxidative stress), were expressed in Nox1-expressing cells, and more than 60% of these returned to normal levels on coexpression of catalase. Thus, H2O2 in low concentrations functions as an intracellular signal that triggers a genetic program related to cell growth.
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