Emodin Inhibits Migration and Invasion of Human Endometrial Stromal Cells by Facilitating the Mesenchymal–Epithelial Transition Through Targeting ILK

• Published in: Reproductive sciences (Thousand Oaks, Calif.) Vol. 23; no. 11; pp. 1526 - 1535
• Main Authors: Zheng, Qiaomei, Xu, Ying, Lu, Jingjing, Zhao, Jing, Wei, Xuan, Liu, Peishu
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.11.2016; Springer International Publishing
• Subjects: Cell Movement - drug effects; Cell Proliferation - drug effects; Embryology; Emodin - administration & dosage; Endometriosis - enzymology; Endometriosis - physiopathology; Endometrium - drug effects; Endometrium - enzymology; Endometrium - physiology; Epithelial-Mesenchymal Transition - drug effects; Female; Humans; Medicine & Public Health; Obstetrics/Perinatology/Midwifery; Original Article; Protein Serine-Threonine Kinases - metabolism; Reproductive Medicine; Stromal Cells - drug effects; Stromal Cells - enzymology; Stromal Cells - physiology; endometriosis; migration; ILK; invasion; MET; emodin
• ISSN: 1933-7191; 1933-7205
• DOI: 10.1177/1933719116645192

Objective: To determine whether emodin facilitates the mesenchymal–epithelial transition (MET) of endometrial stromal cells (ESCs) as well as to explore the mechanism through which emodin favored the MET of ESCs. Methods: Cell viability was tested by methyl thiazolyl tetrazolium assay. Cell migration and invasion abilities were detected by transwell assays. Levels of integrin-linked kinase (ILK) and epithelial–mesenchymal transition (EMT)-related proteins were detected by Western blot. Results: Upregulated ILK and increased abilities of migration and invasion were confirmed in the eutopic and ectopic ESCs (EuSCs and EcSCs), especially in the EcSCs. After treated with emodin, the expression of ILK was statistically downregulated in EcSCs, resulting in the MET and decreased migration and invasion abilities of EcSCs. Additionally, silencing of the ILK gene in EcSCs also achieved the above-mentioned effects, which were strengthened by emodin. Furthermore, exogenous expression of ILK in control ESCs (CSCs) resulted in the EMT and increased abilities of migration and invasion of CSCs, which can be abrogated by emodin. Besides, exogenous expression of ILK also abrogated the effects of emodin on CSCs. Conclusion: Emodin inhibits the migration and invasion abilities of human ESCs by facilitating the MET through targeting ILK.