Melatonin inhibits 17β-estradiol-induced migration, invasion and epithelial-mesenchymal transition in normal and endometriotic endometrial epithelial cells

Abstract Background Melatonin is a potential therapeutic agent for endometriosis, but its molecular mechanism is unclear. Here, we investigated the effect of melatonin on the epithelial-mesenchymal transition (EMT) in endometriotic endometrial epithelial cells and explored the pathway that might be...

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Main Authors: Shasha Qi (Author), Lei Yan (Author), Zhao Liu (Author), Yu-lan Mu (Author), Mingjiang Li (Author), Xingbo Zhao (Author), Zi-Jiang Chen (Author), Hui Zhang (Author)
Format: Book
Published: BMC, 2018-06-01T00:00:00Z.
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001 doaj_f55a8f4b95514f3e8b4afdfb8f2a3bf0
042 |a dc 
100 1 0 |a Shasha Qi  |e author 
700 1 0 |a Lei Yan  |e author 
700 1 0 |a Zhao Liu  |e author 
700 1 0 |a Yu-lan Mu  |e author 
700 1 0 |a Mingjiang Li  |e author 
700 1 0 |a Xingbo Zhao  |e author 
700 1 0 |a Zi-Jiang Chen  |e author 
700 1 0 |a Hui Zhang  |e author 
245 0 0 |a Melatonin inhibits 17β-estradiol-induced migration, invasion and epithelial-mesenchymal transition in normal and endometriotic endometrial epithelial cells 
260 |b BMC,   |c 2018-06-01T00:00:00Z. 
500 |a 10.1186/s12958-018-0375-5 
500 |a 1477-7827 
520 |a Abstract Background Melatonin is a potential therapeutic agent for endometriosis, but its molecular mechanism is unclear. Here, we investigated the effect of melatonin on the epithelial-mesenchymal transition (EMT) in endometriotic endometrial epithelial cells and explored the pathway that might be involved. Methods This hospital-based study included 60 women of reproductive age using the endometrium for immunohistochemistry, 6 women of reproductive age undergoing bilateral tubal ligation and 6 patients with endometriosis for isolation of endometrial epithelial cells or subsequent analysis, respectively. We examined the expression of Notch1/Numb signaling and EMT markers by immunohistochemistry analysis and western blot analysis, the invasion and migration of endometrial epithelial cells by transwell assays, and the cell proliferation by CCK8 assays. Results Compared with normal endometrium, the endometriotic eutopic endometrium showed increased expression of Notch1, Slug, Snail, and N-cadherin, and decreased expression of E-cadherin and Numb. Melatonin or Notch inhibition by specific inhibitor blocked 17β-estradiol-induced cell proliferation, invasion, migration and EMT-related markers in both normal and endometriotic epithelial cells. Conclusions Our data suggest that aberrant expression of Notch1/Numb signaling and the EMT is present in endometriotic endometrium. Melatonin may block 17β-estradiol-induced migration, invasion and EMT in normal and endometriotic epithelial cells by upregulating Numb expression and decreasing the activity of the Notch signaling pathway. 
546 |a EN 
690 |a Endometrial epithelial cells 
690 |a Melatonin 
690 |a 17β-estradiol 
690 |a Migration and invasion 
690 |a Epithelial-mesenchymal transition 
690 |a Gynecology and obstetrics 
690 |a RG1-991 
690 |a Reproduction 
690 |a QH471-489 
655 7 |a article  |2 local 
786 0 |n Reproductive Biology and Endocrinology, Vol 16, Iss 1, Pp 1-12 (2018) 
787 0 |n http://link.springer.com/article/10.1186/s12958-018-0375-5 
787 0 |n https://doaj.org/toc/1477-7827 
856 4 1 |u https://doaj.org/article/f55a8f4b95514f3e8b4afdfb8f2a3bf0  |z Connect to this object online.