Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, 635 Barnhill Drive, MS 4053, Indianapolis, IN 46202, USA.
Anticancer Res. 2010 Jul;30(7):2577-81.
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.
超氧化物歧化酶 1（SOD1）的过表达已被证明是导致卵巢癌顺铂耐药的因素之一。降低 SOD1 的表达有望至少部分恢复卵巢癌化疗中顺铂的敏感性。在这里，我们探讨了 RNAi 作为逆转顺铂耐药性的治疗方法的潜力。
合成 SOD1 特异性小干扰 RNA（siRNA），并在 15μM 顺铂处理前转染至顺铂耐药细胞系 A2780/CP。通过集落形成实验评估细胞存活情况。
与未用 siRNA 处理或用乱序 siRNA 处理的对照细胞相比，用 SOD1 特异性 siRNA 处理的 A2780/CP 细胞对顺铂的敏感性增强。
特异性靶向 SOD1 可能导致顺铂耐药卵巢癌细胞的敏感性增加，SOD1 可作为化疗增敏剂的潜在靶标。
