Volume 30, Issue 2, 2021
DOI: 10.24205/03276716.2020.4076
STUDY ON ASIATICOSIDE INHIBITING 17?-ESTRADIOL-INDUCED EPITHELIAL-MESENCHYMAL TRANSITION BY UP-REGULATING NUMB EXPRESSION AND DOWN-REGULATING NOTCHL PATHWAY
Abstract
Objective: Endometriosis is a benign disease with malignant biological manifestations of metastasis and invasion. The present experiment explored the effect of Asiaticoside on EMT of glandular epithelial cells in endometriosis, and further investigated the signaling pathways that may be involved.
Methods: The endometrial tissues of 60 fertile women were obtained. Immunohistochemical analysis was performed to detect the expressions of Notchl/Numb signaling pathway and EMT-related indicators in normal endometrial tissue and endometriosis eutopic endometrial tissue. The eutopic endometrium of normal patients and endometriosis patients were subjected to primary isolation and culture of glandular epithelial cells, and the effect of epithelial cell proliferation was detected by the CCK-8 method. Transwell test was conducted to detect the influence of epithelial cell migration and invasion. Western blot method was applied to detect the Notchl/Numb signaling pathway and EMT-related proteins.
Results:The expression levels of Notchl, Slug, Snail and N-cadherin proteins in the eutopic endometrial tissue of endometriosis were significantly increased, while the expression levels of E-cadherin and Numb proteins presented a decreasing trend. Asiaticoside and Notch pathway specific inhibitors significantly inhibited the proliferation, migration, invasion and expression of EMT-related indicators of normal and endometriotic eutopic endometrial gland epithelial cells.
Conclusion: Abnormal Notchl/Numb signaling pathway and its EMT exist in endometriosis. Asiaticoside inhibits the epithelial-mesenchymal transition induced by 17?-estradiol through up-regulating the expression of Numb and down-regulating the activity of the Notchl pathway.
Keywords
Endometriosis; Asiaticoside; Notchl/Numb; EMT; 17?-estradiol