Abstract
Endometriosis is an estrogen dependent disease, which is related to infertility. Decidualization is a prerequisite for successful implantation of human embryos, and endometriosis affects the occurrence of decidualization. However, the mechanism that affects decidualization in endometriosis is not fully understood. Here, we find that Aurora kinase A (AURKA) is upregulated in the eutopic endometrium of endometriosis. AURKA inhibits the decidualization of stromal cells in the eutopic endometrium of endometriosis. Furthermore, in animal experiments, AURKA promotes endometriosis and inhibits decidualization in mice with endometriosis, leading to decreased expression of decidualization markers, such as prolactin (PRL), insulin-like growth factor-binding protein-1 (IGFBP1) and desmin. Afterwards, we find that nuclear factor-κB (NF-κB) p65 is a new substrate of AURKA. AURKA interaced with p65 to promoted its phosphorylation and nuclear translocation. Meanwhile, AURKA enhances the protein stability of p65 by prolonging its half-life. In summary, AURKA inhibits the decidualization of the eutopic endometrium in patients with endometriosis by regulating p65, which may provide new ideas for improving decidualization defect in patients with endometriosis.
Published Version
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