Knock-down of Superoxide Dismutase 1 Sensitizes Cisplatin-resistant Human Ovarian Cancer Cells

Overexpression of superoxide dismutase 1 (SOD1) has been shown to be one of the factors involved in causing cisplatin resistance in ovarian cancer. Reduction of SOD1 expression is expected to restore, at least partially, cisplatin sensitivity in ovarian cancer chemotherapy. Here, we explored the pot...

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Bibliographic Details
Published in:Anticancer research 2010-07, Vol.30 (7), p.2577-2581
Main Authors: JONG WON KIM, SAHM, Heather, YOU, Jinsam, MU WANG
Format: Article
Language:English
Subjects:
Antineoplastic Agents - pharmacology
Biological and medical sciences
Cell Line, Tumor
Cisplatin - pharmacology
Drug Resistance, Neoplasm
Female
Female genital diseases
Gene Knockdown Techniques - methods
Gynecology. Andrology. Obstetrics
Humans
Medical sciences
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - enzymology
Ovarian Neoplasms - genetics
RNA, Small Interfering - genetics
Superoxide Dismutase - biosynthesis
Superoxide Dismutase - deficiency
Superoxide Dismutase - genetics
Superoxide Dismutase-1
Transfection
Tumors
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Summary:Overexpression of superoxide dismutase 1 (SOD1) has been shown to be one of the factors involved in causing cisplatin resistance in ovarian cancer. Reduction of SOD1 expression is expected to restore, at least partially, cisplatin sensitivity in ovarian cancer chemotherapy. Here, we explored the potential of RNAi as a therapy for reversal of cisplatin resistance. SOD1-specific small-interfering RNA (siRNA) was synthesized and transfected into cisplatin-resistant cell line A2780/CP prior to treatment with 15 muM cisplatin. Cell survival was assessed by clonogenic assay. An enhanced cisplatin sensitivity was observed in the A2780/CP cells treated with SOD1-specific siRNA, compared to non-siRNA-treated or scrambled-siRNA-treated control cells. Specifically targeting SOD1 could lead to sensitization of cisplatin-resistant ovarian cancer cells, and SOD1 may be used as a potential target for chemosensitizers.
ISSN:0250-7005
1791-7530