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

The present study aimed to investigate the effect and mechanism of the downregulation of PRDX3 on cisplatin‐induced ovarian cancer cell apoptosis



Scholarcy highlights

  • Ovarian cancer continues to be the most frequent cause of cancer mortality among females in Western Europe and theKey words: peroxiredoxins, PRDX3, cisplatin, ovarian cancer, NF‐κBUnited States, with the highest mortality rate of all gynecological malignancies
  • PRDX3 was heavily stained in the cytoplasm and nuclei of the cancer tissues, but little staining was observed in the adjacent non‐cancerous tissues
  • Serous ovarian cancer mostly presented at Federation of Gynaecologists and Obstetricians stage III or IV and a significant difference was observed between stages I + II and III + IV in the various types of ovarian cancer
  • With regard to tumor differentiation, significant differences were identified in the PRDX3 expression among the well‐differentiated, moderately‐differentiated and poorly‐differentiated serous ovarian cancer samples
  • Slight differences in the PRDX3 expression were observed with respect to the histological subtype, age at first diagnosis and lymph node metastasis
  • FIGO stage IV/metastatic serous ovarian cancer samples were shown to overexpress PRDX3 at the highest level, which suggested that the PRDX3 expression was significantly associated with increasing cancer progression
  • As a significant cellular antioxidant, PRDX3 may regulate the physiological levels of H2O2, protecting cells against the apoptosis caused by high levels of H2O2
  • These results suggest that silencing the expression of PRDX3 may enhance cisplatin‐induced ovarian cancer cell apoptosis through the suppression of the NF‐κB signaling pathway

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