J Cancer 2020; 11(9):2390-2400. doi:10.7150/jca.39892 This issue

Research Paper

Overexpression and biological function of PRDX6 in human cervical cancer

Xiaoli Hu#, Ermei lu#, Chunyu Pan, Yichi Xu, Xueqiong Zhu

Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China.
# These authors contributed equally to this work.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Hu X, lu E, Pan C, Xu Y, Zhu X. Overexpression and biological function of PRDX6 in human cervical cancer. J Cancer 2020; 11(9):2390-2400. doi:10.7150/jca.39892. Available from https://www.jcancer.org/v11p2390.htm

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Background: Our previous study demonstrated that the peroxiredoxin 6 (PRDX6) protein was downregulated in squamous cervical cancer samples after neoadjuvant chemotherapy compared with the expression level before chemotherapy. However, the effect of PRDX6 on the biological behavior of cervical cancer is still uncertain. Thus, the purpose of this study was to explore the functional impacts of PRDX6 gene on the biological behavior of cervical squamous cancer cells.

Methods: An immunofluorescence assay was applied to evaluate the expression difference of PRDX6 between cervical cancer tissue and normal cervical tissue samples. A lentivirus was used to upregulate and downregulate PRDX6 expression in SiHa cells. Furthermore, the role of PRDX6 on cell proliferation, apoptosis, migration and invasion was evaluated. Additionally, the effect of PRDX6 on the progression of the cervical cancer was investigated via a xenograft model in BALB/c nude mice that either overexpressed or underexpressed PRDX6.

Results: The expression of PRDX6 was generally increased in cervical cancer tissues. Furthermore, the overexpression of PRDX6 stimulated the proliferation, migration and invasion of cervical squamous cancer cells, and suppressed cell apoptosis. The opposite results were also obtained after successful knockdown of PRDX6. In addition, the overexpression of PRDX6 significantly promoted the growth of cervical carcinoma in vivo.

Conclusions: PRDX6 promoted the proliferation, migration and invasion, and inhibited apoptosis in cervical cancer cells, indicating that PRDX6 is an important promoter of cervical cancer tumorigenicity.

Keywords: PRDX6, cervical cancer, proliferation, migration, invasion, apoptosis