J Cancer 2020; 11(10):2821-2829. doi:10.7150/jca.39269

Research Paper

Dysbindin facilitates invasion and metastasis by promoting phosphorylation of ERK in epithelial ovarian cancer

Xiaohui Lv1, Xin Guo2,3, Yi Ru4, Fuxing Zhou1, Xiaoshan Yang5, Junli Ge1, Jia Li1, Shujuan Liu1, Kuo Jiang6✉, Biliang Chen1✉

1. Department of Gynecology and Obstetrics, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
2. Department of General Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China.
3. Department of Endoscopic Surgery, Chinese People's Liberation Army 986 th Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710054, China.
4. Department of biochemistry and molecular biology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
5. State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi International Joint Research Center for Oral Diseases, Center for Tissue Engineering, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
6. Department of Spine Surgery, Honghui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710054, China.

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Citation:
Lv X, Guo X, Ru Y, Zhou F, Yang X, Ge J, Li J, Liu S, Jiang K, Chen B. Dysbindin facilitates invasion and metastasis by promoting phosphorylation of ERK in epithelial ovarian cancer. J Cancer 2020; 11(10):2821-2829. doi:10.7150/jca.39269. Available from http://www.jcancer.org/v11p2821.htm

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Abstract

Dysbindin has been reported to be correlated with several malignancies. However, the clinical significance and biological role of dysbindin in epithelial ovarian cancer remains largely unknown. Here we demonstrated that the mRNA and protein levels of dysbindin were significantly upregulated in EOC tissues compared with normal ovarian tissues. High levels of dysbindin were significantly correlated with worse clinicopathological characteristics and poor prognosis in EOC patients. Overexpression and silencing of dysbindin promoted and inhibited, respectively, invasion and metastasis of EOC cells in vitro and in vivo. Mechanistically, dysbindin activates phosphorylation of ERK to promote the epithelial-mesenchymal transition and to mediate the invasive and metastatic ability of EOC cells. Our findings suggest that dysbindin facilitates invasion and metastasis by promoting the EMT of EOC cells and may serve as a potential therapeutic target in EOC.

Keywords: Dysbindin, EMT, ERK, Invasion, Metastasis