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miR-370-3p 通过下调子宫内膜间质细胞中 EDN1 的表达抑制人子宫内膜异位症的发展。

MiR-370-3p inhibits the development of human endometriosis by downregulating EDN1 expression in endometrial stromal cells.

机构信息

Department of Interventional Radiology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, Jiangsu, China.

Department of Pathology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, Jiangsu, China.

出版信息

Cell Biol Int. 2021 Jun;45(6):1183-1190. doi: 10.1002/cbin.11552. Epub 2021 Mar 26.

DOI:10.1002/cbin.11552
PMID:33470475
Abstract

MiR-370-3p has been demonstrated to be downregulated in patients with endometriosis (EM). However, its role and molecular mechanisms in the progression of EM remain unclear. Real-time polymerase chain reaction was used to measure the expression of miR-370-3p and endothelin-1 (EDN1) in patients with or without EM. After miR-370-3p overexpression or knockdown in ectopic endometrial hEM15A cells, the changes in the proliferation, apoptosis, and migration and invasion capacities were detected by using cell counting kit-8, flow cytometry, and transwell methods. The interplay between miR-370-3p and EDN1 was confirmed by a luciferase reporter assay. Patients with EM showed adverse expression of EDN1 and miR-370-3p, especially in eutopic endometrium and ectopic endometrium. MiR-370-3p inhibited the proliferation, metastasis, and invasion capacities of hEM15A cells and promoted apoptosis. Investigation of its molecular mechanism revealed that miR-370-3p targeted EDN1 to influence the biological functions of hEM15A cells. MiR-370-3p represented as a therapeutic target for EM treatment.

摘要

miR-370-3p 在子宫内膜异位症(EM)患者中表现为下调。然而,其在 EM 进展中的作用和分子机制尚不清楚。实时聚合酶链反应用于测量 EM 患者和非 EM 患者中 miR-370-3p 和内皮素-1(EDN1)的表达。在异位子宫内膜 hEM15A 细胞中转染 miR-370-3p 过表达或敲低后,通过细胞计数试剂盒-8、流式细胞术和 Transwell 方法检测细胞增殖、凋亡、迁移和侵袭能力的变化。通过荧光素酶报告基因检测证实了 miR-370-3p 和 EDN1 之间的相互作用。EM 患者表现出 EDN1 和 miR-370-3p 的异常表达,尤其是在位和异位子宫内膜。miR-370-3p 抑制 hEM15A 细胞的增殖、转移和侵袭能力,并促进凋亡。对其分子机制的研究表明,miR-370-3p 靶向 EDN1 影响 hEM15A 细胞的生物学功能。miR-370-3p 可作为治疗 EM 的靶点。

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