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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.

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