[Estrogen, estrogen receptor and miR-21 in adenomyosis: their pathogenic roles and regulatory interactions]

Zeng Y, Y Zeng, Yulan Zeng, Jia J, J Jia, Jianping Jia, J Lu, Juan Lü, Lu J, C Zeng, Zeng C, Cheng Zeng, H Geng, Geng H, Hui Geng, Yao Chen, Y. Chen, Chen Y
Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024 · vol. 44(4) , pp. 627–635 · doi:10.12122/j.issn.1673-4254.2024.04.02 · PMID:38708494 · PMC11073943 · W4396676667
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that miR-21, estrogen, and estrogen receptor are involved in adenomyosis pathogenesis, with miR-21 promoting cell proliferation, migration, and inhibiting apoptosis by altering cell ultrastructure.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

The study investigated the mechanistic roles and regulatory interactions of miR-21, estrogen (E2), and estrogen receptors (ER) in adenomyosis. miR-21 levels were measured by qRT-PCR in adenomyosis lesion tissues versus cervical lesion controls, and in primary cultured adenomyosis cells under E2 activation, E2 deprivation, and ER inhibition conditions, followed by miR-21 overexpression or inhibition to assess effects on proliferation, apoptosis, migration, and ultrastructural changes. miR-21 was higher in adenomyosis lesions than in normal myometrium, increased with E2 activation when ER was not inhibited, decreased when E2 deprivation was combined with ER inhibition, and functional manipulation of miR-21 altered cell proliferation/migration and mitochondrial/endoplasmic reticulum/lysosomal-autophagy-related ultrastructure, with miR-21 inhibition promoting apoptosis and miR-21 overexpression reversing these effects; the authors additionally note that ER may regulate miR-21 through pathways beyond E2 binding. This paper is centrally about adenomyosis — it focuses on how miR-21 is regulated by estrogen and ER and how this relates to adenomyosis cell behavior and ultrastructural changes.

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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 antiapoptosis 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.
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南方医科大学学报 ›› 2024, Vol. 44 ›› Issue (4): 627-635.doi: 10.12122/j.issn.1673-4254.2024.04.02 曾玉燕，贾金金，卢 洁，曾 诚，耿红玲，陈 颐 - 广州中医药大学第二附属医院妇科，广东 广州 510120；广州中医药大学第一附属医院妇科，广东 广州 510405 ZENG Yuyan, JIA Jinjin, LU Jie, ZENG Cheng, GENG Hongling, CHEN Yi - Department of Gynecology, Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China; Department of Gynecology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China 摘要： 目的 探讨miR-21、雌激素（E2）及其受体（ER）在子宫腺肌病发病中的具体机制。方法 采用qRT-PCR检测miR-21在子宫腺肌病组织中水平，以宫颈病变为对照组。体外原代培养子宫腺肌病细胞，qRT-PCR检测E2激活组、ICI82780（ER抑制剂）+E2激活组、E2剥夺组、E2剥夺+ER抑制组及对照组各组miR-21水平。miR-21 mimic、miR-21 inhibitor转染子宫腺肌病细胞，分别过表达和干扰miR-21，从正反两方面验证miR-21对子宫腺肌病细胞增殖、凋亡、迁移及细胞自噬等超微结构的影响。结果 miR-21在子宫腺肌病病灶组织中的表达水平明显高于正常子宫肌层中表达水平（P0.05）；E2激活状态下，E2激活组miR-21表达水平较ER抑制+E2激活组及对照组升高（P<0.05）；E2剥夺状态下，E2剥夺+ER抑制组miR-21表达水平较E2剥夺组及对照组降低（P<0.05）；干扰miR-21可以抑制子宫腺肌病细胞增殖和迁移，使线粒体内质网不同程度扩张、溶酶体增多、自噬小体出现，促进细胞的凋亡；而过表达miR-21则发挥相反的作用。结论 MiR-21在子宫腺肌病细胞中通过改变细胞超微结构而发挥促增殖、迁移及抗凋亡的作用，可能与疾病的早期形成有关；ER除与E2结合调控miR-21外还可通过其他途径调控miR-21，这可能是子宫腺肌病的发病机制之一，其中ER对miR-21的调控作用大于E2。

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis

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chemicals 2
estrogen estrogen

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