Decreased expression of peroxiredoxin1 inhibits proliferation, invasion, and metastasis of ovarian cancer cell
Received 23 May 2018
Accepted for publication 10 September 2018
Published 2 November 2018 Volume 2018:11 Pages 7745—7761
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 4
Editor who approved publication: Dr William Cho
Ming-Jun Zheng,1,2,* Jing Wang,1,2,* Hui-Min Wang,1,2 Ling-Ling Gao,1,2 Xiao Li,1,2 Wen-Chao Zhang,1,2 Rui Gou,1,2 Qian Guo,1,2 Xin Nie,1,2 Juan-Juan Liu,1,2 Bei Lin1,2
1Department of Gynaecology and Obstetrics, Shengjing Hospital Affiliated to China Medical University, Heping District, Shenyang 110004, Liaoning, China; 2Key Laboratory of Maternal-Fetal Medicine of Liaoning Province, Key Laboratory of Obstetrics and Gynecology of Higher Education of Liaoning Province, Liaoning, China
*These authors contributed equally to this work
Aim: The aim of this study was to explore the expression of peroxiredoxin1 (PRDX1) in epithelial ovarian cancer, analyze the relationship between PRDX1 and clinicopathologic parameters of patients with ovarian cancer, including their prognosis, and describe changes and the mechanisms involved in malignant biologic behavior of ovarian cancer cells when PRDX1 expression is inhibited.
Methods: The expression of PRDX1 was detected immunohistochemically in 15 samples of normal ovarian tissue, 21 benign, 11 borderline, and 101 malignant epithelial ovarian tumors. Changes in ovarian cancer cell proliferation, invasion, and metastasis before and after inhibiting PRDX1 expression were assessed by cell function assay. Additionally, gene set enrichment analysis (GSEA) of PRDX1 was performed by the Cancer Genome Atlas database. A protein–protein interaction network was then constructed and a pathway function analysis of the genes in the network was conducted.
Results: PRDX1 expression was mainly localized to the cytoplasm, as well as the nucleus of cells. The expression rate of PRDX1 in epithelial ovarian malignant tissues (96.04%) was significantly higher than that in borderline (72.72%) and benign (57.14%) epithelial ovarian tumors, and normal ovarian tissue (20%; all P<0.05). Cox multivariate regression analysis indicated that advanced clinical stage, low tissue differentiation, and high expression of PRDX1 were independent risk factors affecting the prognosis of epithelial ovarian cancer (all P<0.05). Cell function assay verified that the decreased expression of PRDX1 inhibited ovarian cancer cell proliferation, invasion, and metastasis. GSEA analysis indicated that PRDX1 was significantly related to the Wnt signaling pathway. Western blot analysis confirmed that PRDX1 could regulate the expression of β-catenin in the Wnt pathway.
Conclusion: Decreased expression of PRDX1 can attenuate cell proliferation, invasion, and metastasis of ovarian cancer cells. The expression of PRDX1 is related to the prognosis of patients with ovarian cancer and can therefore be used as a biomarker.
Keywords: epithelial ovarian cancer, peroxiredoxin1, immunohistochemistry, invasion, metastasis, pathways
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