Emodin Reverses the Epithelial–Mesenchymal Transition of Human Endometrial Stromal Cells by Inhibiting ILK/GSK-3β Pathway

Qiaomei Zheng, Jinhua Wang, Wenwen Li, Xiaoyun Chen, Shaozhan Chen, Lihong Chen
Drug design, development and therapy · 2020 · vol. Volume 14 , pp. 3663–3672 · doi:10.2147/dddt.s262816 · PMID:32982173 · PMC7490435 · W3083872588
article OA: gold CC0 ⤵ 8 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

Emodin reversed the epithelial-mesenchymal transition of human endometrial stromal cells by inhibiting the ILK/GSK-3β pathway, thus down-regulating their migration and invasion.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This study investigated how emodin affects migration and invasion of human endometriosis endometrial stromal cells (EESs) compared with control endometrial stromal cells (CESs), using transwell assays and protein analyses (Western blot) in samples from 15 women with endometriosis and 12 without. Emodin significantly reduced migration and invasion in both cell types and was associated with decreased ILK and phosphorylated GSK-3β, alongside reversal of EMT markers (increased keratin, decreased vimentin, β-catenin, and slug in a dose- and time-dependent manner). Mechanistically, ILK knockdown in EESs mimicked the emodin effects and ILK overexpression in CESs increased p-GSK-3β and EMT-related signaling, while pharmacologic modulation via SB216763 altered EMT through p-GSK-3β/β-catenin/slug and these effects were abrogated by emodin; the paper’s caveat is that it is conducted in cultured cells rather than in vivo. This paper is centrally about endometriosis — it tests emodin’s ILK/GSK-3β–mediated reversal of EMT to explain reduced invasiveness of endometriosis endometrial stromal cells.

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Abstract

PURPOSE: To explore the exact mechanism through which emodin down-regulates the migration and invasion abilities of endometrial stromal cells. Moreover, to explore the theoretical basis of emodin in the treatment of endometriosis. PATIENTS AND METHODS: Endometriosis endometrial stromal cells (EESs) were cultured from 15 women with endometriosis and control endometrial stromal cells (CESs) were cultured from 12 women without endometriosis. The levels of proteins were evaluated by Western blot. The migration and invasion abilities of cells were detected by transwell assays. RESULTS: The abilities of migration and invasion of EESs were much stronger than those of CESs. After treated with emodin, the migration and invasion abilities of EESs and CESs were significantly down-regulated, and the levels of integrin-linked kinase (ILK) and p-GSK-3β were statistically down-regulated in EESs. Besides that, the expression of keratin was up-regulated while the expression of vimentin, β-catenin and slug were all down-regulated by emodin in a dose- and time-dependent manner. Silencing of ILK gene in EESs also achieved the above effects, which were strengthened by emodin. Conversely, exogenous expression of ILK in CESs increased the expression of p-GSK-3β, which were abrogated by emodin. Furthermore, SB216763 increased migration and invasion abilities of CESs by facilitating the epithelial-mesenchymal transition (EMT) through up-regulating levels of p-GSK-3β, β-catenin and slug, which were also abrogated by emodin. CONCLUSION: Emodin inhibits the migration and invasion abilities of human endometrial stromal cells by reversing the EMT via ILK/GSK-3β pathway. So, emodin may be considered as a promising targeted therapy for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Emodin Endometriosis Endometrium Glycogen Synthase Kinase 3 beta Protein Serine-Threonine Kinases Stromal Cells Cell Movement Cell Movement Cells, Cultured Emodin Endometriosis Endometriosis Endometriosis Endometrium Endometrium Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Female Glycogen Synthase Kinase 3 beta Glycogen Synthase Kinase 3 beta

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