Abstract
We examined the involvement of peroxiredoxin 6 (Prdx 6) in providing chemoprotection against cisplatin cytotoxicity in SKOV-3 ovarian cancer cells. Treatment of SKOV-3 cells with cisplatin-induced cytotoxicity that was associated with increased accumulation of intracellular reactive oxygen species (ROS) and apoptosis mediated by proteolytically activated caspase 3 and 9. Overexpression of Prdx 6 protein or exposure to N-acetylcysteine (NAC) reversed the apoptotic effect of cisplatin by reducing ROS levels and suppressing the caspase signaling pathway. These results indicate that targeting Prdx 6 may sensitize cancer cells to ROS-producing therapeutic treatments, such as anticancer drugs and radiation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcysteine / pharmacology
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Antineoplastic Agents / pharmacology*
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Antioxidants / pharmacology
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Apoptosis / drug effects*
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Caspase 3 / metabolism
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Caspase 9 / metabolism
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Cell Line, Tumor
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Cell Survival / drug effects
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Cisplatin / pharmacology*
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Dose-Response Relationship, Drug
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Drug Resistance, Neoplasm
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Enzyme Activation
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Female
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Humans
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Ovarian Neoplasms / genetics
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Ovarian Neoplasms / metabolism*
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Ovarian Neoplasms / pathology
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Peroxiredoxin VI / genetics
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Peroxiredoxin VI / metabolism*
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Reactive Oxygen Species / metabolism
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Signal Transduction / drug effects
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Time Factors
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Transfection
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Up-Regulation
Substances
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Antineoplastic Agents
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Antioxidants
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Reactive Oxygen Species
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PRDX6 protein, human
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Peroxiredoxin VI
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CASP3 protein, human
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CASP9 protein, human
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Caspase 3
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Caspase 9
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Cisplatin
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Acetylcysteine