siRNA targeting of PRDX3 enhances cisplatin-induced apoptosis in ovarian cancer cells through the suppression of the NF-κB signaling pathway

Abstract

The overexpression of peroxiredoxins (prxs) has been shown to be associated with the development, progression and drug resistance of cancer. However, the role of the prxs in the drug resistance of ovarian cancer is unknown. The present study aimed to investigate the effect and mechanism of the downregulation of PRDX3 on cisplatin‑induced ovarian cancer cell apoptosis. The expression of PRDX3 in ovarian cancer was examined by immunohistochemistry. The effect on cisplatin‑induced ovarian cancer apoptosis by the silencing of PRDX3 was determined by cell proliferation and colony formation assays and the examination of tumor growth in the nude mice. To further investigate the mechanism behind the downregulation of PRDX3, the expression of the anti‑apoptotic proteins Bcl‑2 and Bcl‑XL and the pro‑apoptotic proteins Bax, Caspase‑3 and Caspase‑9 was examined in various ovarian cancer cells. The results showed that the aberrant expression of PRDX3 in ovarian cancer may be a factor responsible for its progression. SKOV3 ovarian cancer cells transfected with PRDX3/small interfering (Si)‑1 efficiently downregulated the expression of PRDX3 and thus decreased the growth of the SKOV3 cells in vitro and in vivo. Furthermore, the silencing of PRDX3 triggered cisplatin‑mediated apoptosis in the ovarian cancer cells, which may act through suppression of the NF‑κB signaling pathway. These data suggest a new mechanism by which the downregulation of PRDX3 enhances cisplatin‑induced ovarian cancer cell apoptosis. This mechanism may provide new evidence for the potential application of PRDX3‑siRNA in ovarian cancer therapy.