Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 130, Issue 5, Pages 1071-1081Publisher
WILEY
DOI: 10.1002/ijc.26079
Keywords
MnSOD; apolipoprotein A-I; mimetic peptides; oxidative stress; animal models; epithelial ovarian cancer
Categories
Funding
- USPHS [HL-30568, HL-082823]
- Womens Endowment
- Carl and Roberta Deutsch Family Foundation
- Joan English Fund for Women's Cancer Research
- Ovarian Cancer Coalition
- Helen Beller Foundation
- Wendy Stark Foundation
- Sue and Mel Geleibter Family Foundation
- VA Merit I Award
- Sue and Mel Geleibter Family Foundation USPHS [HL-30568, HL-082823]
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We recently reported that apoA-I and apoA-I mimetic peptides prevent the development of flank tumors in immunocompetent C57BL/6J mice. To delineate the mechanism(s) of action of apoA-I mimetic peptides in tumor development, we examined the effect of D-4F (an apoA-I mimetic peptide) on the antioxidant status and on the gene expression and function of antioxidant enzymes in ID8 cells (a mouse epithelial ovarian cancer cell line) and in a mouse model. We demonstrate that D-4F treatment significantly reduces the viability and proliferation of ID8 cells, with a concomitant improvement of the antioxidant status of ID8 cells as measured by lipid peroxidation, protein carbonyl, superoxide anion, and hydrogen peroxide levels. D-4F treatment induces MnSOD (but not CuZnSOD) mRNA, protein, and activity. Inhibition of MnSOD in ID8 cells using shRNA vectors abrogates the inhibitory effects of D-4F on ID8 cell viability and proliferation. Moreover, tumor development from ID8 cells carrying shRNA for MnSOD were unaffected by D-4F treatment. Our results suggest that the inhibitory effects of D-4F on ID8 cell proliferation and tumor development are mediated, at least in part, by the induced expression and activity of MnSOD.
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