Estrogen, estrogen receptor and miR-21 in adenomyosis: their pathogenic roles and regulatory interactions
10.12122/j.issn.1673-4254.2024.04.02
- VernacularTitle:子宫腺肌病组织中的雌激素、雌激素受体、miR-21:致病作用和调控作用
- Author:
Yuyan ZENG
1
;
Jinjin JIA
;
Jie LU
;
Cheng ZENG
;
Hongling GENG
;
Yi CHEN
Author Information
1. 广州中医药大学第二附属医院妇科,广东 广州 510120
- Keywords:
adenomyosis;
miR-21;
estrogen;
estrogen receptor
- From:
Journal of Southern Medical University
2024;44(4):627-635
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the pathogenic roles of miR-21, estrogen (E2), and estrogen receptor (ER) in adenomyosis. Methods We examined the expression levels of miR-21 in specimens of adenomyotic tissue and benign cervical lesions using qRT-PCR. In primary cultures of cells isolated from the adenomyosis lesions, the effect of ICI82780 (an ER inhibitor) on miR-21 expression levels prior to E2 activation or after E2 deprivation were examined with qRT-PCR. We further assessed the effects of a miR-21 mimic or an inhibitor on proliferation, apoptosis, migration and autophagy of the cells. Results The expression level of miR-21 was significantly higher in adenomyosis tissues than in normal myometrium (P<0.05). In the cells isolated from adenomyosis lesions, miR-21 expression level was significantly higher in E2 activation group than in ER inhibition+E2 activation group and the control group (P<0.05);miR-21 expression level was significantly lower in cells in E2 deprivation+ER inhibition group than in E2 deprivation group and the control group (P<0.05). The adenomyosis cells transfected with miR-21 inhibitor showed inhibited proliferation and migration, expansion of mitochondrial endoplasmic reticulum, increased lysosomes, presence of autophagosomes, and increased cell apoptosis, while transfection of the cells with the miR-21 mimic produced the opposite effects. Conclusion MiR-21 plays an important role in promoting proliferation, migration, and anti-apoptosis in adenomyosis cells by altering the cell ultrastructure, which may contribute to early pathogenesis of the disease. In addition to binding with E2, ER can also regulate miR-21 through other pathways to participate in the pathogenesis of adenomyosis, thus having a stronger regulatory effect on miR-21 than E2.
