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Nigericin Inhibits Epithelial Ovarian Cancer Metastasis by Suppressing the Cell Cycle and Epithelial–Mesenchymal Transition

Wen Wang1,2, Yan Zhao1,3, Shujuan Yao2, Xiujuan Cui2, Wenying Pan1,4, Wenqian Huang1, Jiangang Gao5, Taotao Dong1*, and Shiqian Zhang1*

1Qilu Hospital, Shandong University, Department of Obstetrics and Gynecology, Jinan, Shandong 250012, P.R. China; E-mail: wangwen20161008@163.com

2Tengzhou Central People’s Hospital, Department of Obstetrics and Gynecology, Tengzhou, Shandong 277500, P.R. China

3Linyi People’s Hospital, Department of Obstetrics and Gynecology, Linyi, Shandong 276000, P.R. China

4Binzhou Medical School Affiliated Hospital, Department of Obstetrics and Gynecology, Binzhou, Shandong, P.R. China

5Shandong University, School of Life Science, Jinan, Shandong, P.R. China

* To whom correspondence should be addressed.

Received December 4, 2016; Revision received May 4, 2017
Epithelial ovarian cancer (EOC) has the highest mortality among various types of gynecological malignancies. Most patients die of metastasis and recurrence due to cisplatin resistance. Thus, it is urgent to develop novel therapies to cure this disease. CCK-8 assay showed that nigericin exhibited strong cytotoxicity on A2780 and SKOV3 cell lines. Flow cytometry indicated that nigericin could induce cell cycle arrest at G0/G1 phase and promote cell apoptosis. Boyden chamber assay revealed that nigericin could inhibit migration and invasion in a dose-dependent manner by suppressing epithelial–mesenchymal transition (EMT) in EOC cells. These effects were mediated, at least partly, by the Wnt/β-catenin signaling pathway. Our results demonstrated that nigericin could inhibit EMT during cell invasion and metastasis through the canonical Wnt/β-catenin signaling pathway. Nigericin may prove to be a novel therapeutic strategy that is effective in patients with metastatic EOC.
KEY WORDS: epithelial ovarian cancer, nigericin, cell cycle, epithelial–mesenchymal transition

DOI: 10.1134/S0006297917080089