Aims: The enhanced ability of endometrial cell migration and invasion is the foundation for formation of ectopic lesions in endometriosis. Ezrin has been reported to regulate cell motility by remodeling the cytoskeleton. However, little is known about the mechanisms through which ezrin remodels the cytoskeleton and cell structure to promote cell motility in endometriosis.
Methods: In our study, expression and distribution of ezrin, and Rho pathway were detected through immunohistochemical analysis. The effects of inhibiting ezrin T567 phosphorylation on Rho signaling pathway and cytoskeleton were investigated through western blot, transmission electron microscopy and immunofluorescence analysis.
Key findings: We found that the expression of ezrin and Rho pathway was higher in ectopic endometrium. NSC305787 inhibited the phosphorylation of ezrin T567, resulting in decreased expression of Rho pathway and reduced filopodia formation in ectopic endometrial stromal cells.
Significance: Taken together, our study suggested that ezrin T567 phosphorylation modulated migration and invasion of ectopic ESCs through actin reconstructions, which may serve as a novel therapeutic target in ovarian endometriosis.
Keywords: Actin cytoskeleton; Cell migration and invasion; Endometrial stromal cells; Ezrin T567 phosphorylation; Filopodia; Ovarian endometriosis; Rho signaling pathway.
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