NEK2 promotes the development of ovarian endometriosis and impairs decidualization by phosphorylating FOXO1

Mengxue Wang, Fangyuan Sun, Shucai Zhang, Xiaohui Zhang, Yujun Sun, Ting Yu, Yuanyuan Li, Aifang Jiang, Pengyun Qiao, Chune Ren, Tingting Yang
Cellular and molecular life sciences : CMLS · 2024 · vol. 81(1) , pp. 237 · doi:10.1007/s00018-024-05270-8 · PMID:38795132 · W4399021788
article OA: gold CC0 ⤵ 10 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

NEK2 promotes ovarian endometriosis development and impairs decidualization by phosphorylating and destabilizing FOXO1, making NEK2 a potential therapeutic target.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated whether NEK2 contributes to ovarian endometriosis and associated defective endometrial decidualization by analyzing NEK2 expression in human endometrial tissues and testing NEK2 effects in endometrial stromal cells and mouse models. NEK2 levels were increased in ectopic and eutopic endometrium from patients with ovarian endometriosis, and NEK2 phosphorylated FOXO1 at Ser184, destabilizing FOXO1 while promoting endometrial cell proliferation, migration, invasion, and impairing decidualization; NEK2 inhibition with INH1 reduced ectopic lesion growth and promoted decidualization in mouse settings. A limitation is that the work relies on in vitro decidualization induction and specific mouse/artificial models rather than direct demonstration of mechanisms across human infertility outcomes. This paper is centrally about endometriosis — it links NEK2-driven FOXO1 phosphorylation to ovarian endometriosis development and impaired endometrial decidualization.

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Abstract

Ovarian endometriosis is a common gynecological disease, and one of its most significant symptoms is infertility. In patients with endometriosis, defects in endometrial decidualization lead to impaired endometrial receptivity and embryo implantation, thus affecting early pregnancy and women's desire to have children. However, the mechanisms underlying the development of endometriosis and its associated defective decidualization are unclear. We find that NEK2 expression is increased in the ectopic and eutopic endometrium of patients with endometriosis. Meanwhile, NEK2 interacts with FOXO1 and phosphorylates FOXO1 at Ser184, inhibiting the stability of the FOXO1 protein. Importantly, NEK2-mediated phosphorylation of FOXO1 at Ser184 promotes cell proliferation, migration, invasion and impairs decidualization. Furthermore, INH1, an inhibitor of NEK2, inhibits the growth of ectopic lesions in mouse models of endometriosis and promotes endometrial decidualization in mouse models of artificially induced decidualization. Taken together, these findings indicate that NEK2 regulates the development of endometriosis and associated disorders of decidualization through the phosphorylation of FOXO1, providing a new therapeutic target for its treatment.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Cell Proliferation Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium

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