Although peroxiredoxin 3 (Prx3) has been reported to be involved in cervical cancer (CC) carcinogenesis, the significance of Prx3 in CC progression remains unclear. The present study was conducted to investigate the expression features of Prx3 to better understand the mechanism of tumor growth and invasion. Sixty-eight patients with invasive squamous cervical cancer were included in the present study. The status of human papillomavirus (HPV) infection was detected by hybridization and quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemistry was performed on paraffin-embedded sections using monoclonal antibodies against Prx3 and Ki67. All samples were positive for high-risk HPV, among which fifty-six samples were positive for HPV16, seven for HPV18 and five for HPV33. The expression of HPV16 E6/E7 was significantly higher in cancer areas compared to the adjacent normal epithelial tissuses. The positive cells for Prx3 and Ki67 were significantly higher in cancer cells compared to normal epitheliums and the staining pattern of Prx3 was consistent with that of Ki67 (Pearson's correlation coefficient was 0.801, P= 0.000). The upregulation of Prx3 might be a protective response to oxidative stress in the cancer microenvironment. The expression consistency of Prx3 and Ki67 suggests Prx3 to be a potential marker for cell proliferation of CC.