1. Academic Validation
  2. MiR-182 inhibits proliferation, migration, invasion and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis

MiR-182 inhibits proliferation, migration, invasion and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis

  • Mol Cell Biochem. 2021 Mar;476(3):1575-1588. doi: 10.1007/s11010-020-03986-2.
Min Wu 1 2 Yi Zhang 3
Affiliations

Affiliations

  • 1 Department of Gynecology and Obstetrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, People's Republic of China.
  • 2 Department of Gynecology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, 410008, Hunan Province, People's Republic of China.
  • 3 Department of Gynecology and Obstetrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, People's Republic of China. zhangyi5588@aliyun.com.
Abstract

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-κB 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-κB 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-κB 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-κB signaling pathway in endometriosis. These results provide new insights into the interaction between miR-182 and NF-κB pathway and their potential as therapeutic targets for treatment of endometriosis.

Keywords

Endometriosis; Inflammation; Invasion; Migration; RELA; miR-182.

Figures
Products