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

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.

LncRNA BANCR Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the miR-15a-5p/TRIM59 Axis

“…Accordingly, the subsequent experiment revealed higher expression levels of lncRNA BANCR in Ect-ESCs relative to eutopic ESCs ( P < 0.05, Figure 1(c) ). Several studies have documented that suppression of abnormal proliferation or invasion of ESCs mitigates EM progression [ 33 – 35 ]. To further explore the role of lncRNA BANCR in ESC proliferation and invasion, Ect-ESCs were transfected with si-BANCR (si-BANCR#1 and si-BANCR#2) to downregulate lncRNA BANCR expression ( P < 0.05, Figure 1(d) ).…”

METTL3 is aberrantly expressed in endometriosis and suppresses proliferation, invasion, and migration of endometrial stromal cells

“…Proliferation, invasion, and migration of ESCs are of vital significance in the onset of EM 23,24 . To assess the functionality of METTL3 on Ect‐ESCs, we successfully upregulated METTL3 in the Ect‐ESCs ( p < 0.01, Figure 2A,B).…”

“…Proliferation, invasion, and migration of ESCs are of vital significance in the onset of EM. 23,24 To assess the functionality of METTL3 on Ect-ESCs, we successfully upregulated METTL3 in the Ect-ESCs (p < 0.01, Figure 2A,B). Our results showed that after METTL3 overexpression, the proliferation potential of Ect-ESCs was significantly reduced (p < 0.01, Figure 2C,D) along with notably decreased numbers of invasive and migrative Ect-ESCs (p < 0.01, Figure 2E,F).…”

Autophagy as a Therapeutic Target of Natural Products Enhancing Embryo Implantation

“…Four compounds, apigenin, curcumin, genistein, and quercetin, were identified as antagonists for embryo implantation [124][125][126][127][128][129][130]. Four compounds, berberine, emodin, paeoniflorin, and γ-tocotrienol, increased implantation rates by increasing endometrial receptivity or decidualization [103,116,120,131,132]. In contrast, resveratrol has been shown to have dual effects as an agonist and antagonist [133,134].…”