期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 476, 期 3, 页码 1575-1588出版社
SPRINGER
DOI: 10.1007/s11010-020-03986-2
关键词
Endometriosis; miR-182; RELA; Inflammation; Migration; Invasion
类别
资金
- Health Commission of Hunan Province [B2017125]
The study revealed that miR-182 targets RELA directly and inhibits the NF-kappa B signaling pathway, thereby attenuating the proliferation, migration, invasion, EMT, and inflammatory response of endometrial stromal cells in endometriosis.
Endometriosis affects about 10-15% women for reproductive age, but it is not currently curable and the underlying etiology for this disease is still not clear. In the present study, functions and mechanisms of miR-182 and RELA in endometriosis were investigated. BAY 11-7082 was used to block NF-kappa B pathway. qRT-PCR, ELISA and western blot assays were employed to evaluate the expressions of miR-182 and RELA, inflammatory factors and epithelial-mesenchymal transition (EMT)-related markers, and activation of NF-kappa B pathway. MTT, wound healing or Transwell assays were used to evaluate the cell proliferation, migration and invasion capacities. Bioinformatic and dual-luciferase reporter assays were carried out to analyze the interaction between miR-182 and RELA. MiR-182 expression was decreased, while RELA was increased as developed from normal to eutopic and ectopic status, which was accompanied by upregulated inflammatory factors and EMT-related proteins. RELA was directly targeted by miR-182 in human endometrial stromal cells. Overexpression of RELA increased inflammation-associated and EMT-related markers expression, while miR-182 upregulation decreased the expression of these genes in a dose-dependent manner, which finally attenuated the proliferation, migration and invasion capacities of endometrial stromal cells through deactivation of NF-kappa B signaling pathway. Moreover, co-overexpression of RELA reversed the above effects induced by miR-182. In a word, miR-182 directly targeted RELA and inhibited proliferation, migration, invasion, EMT and inflammation of endometrial stromal cells through deactivation of NF-kappa B signaling pathway in endometriosis. These results provide new insights into the interaction between miR-182 and NF-kappa B pathway and their potential as therapeutic targets for treatment of endometriosis.
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