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Stem Cell Res Ther. 2019 Sep 23;10(1):287. doi: 10.1186/s13287-019-1388-5.

miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.

Author information

1
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
2
Department of Obstetrics and Gynecology, Zhujiang Hospital of Southern Medical University, No.253, Middle Gongyeda Road, Haizhu District, Guangzhou, 510280, China.
3
Department of Immunology/Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
4
Department of Obstetrics and Gynecology, Shenzhen Maternal and Child Healthcare Hospital of Southern Medical University, Shenzhen, 518028, China.
5
Department of Obstetrics and Gynecology, Zhujiang Hospital of Southern Medical University, No.253, Middle Gongyeda Road, Haizhu District, Guangzhou, 510280, China. mayingwuzhuoyi@126.com.

Abstract

BACKGROUND:

miRNA expression profiles in ectopic endometrium (EC) serving as pathophysiologic genetic fingerprints contribute to determining endometriosis progression; however, the underlying molecular mechanisms remain unknown.

METHODS:

miRNA microarray analysis was used to determine the expression profiling of EC fresh tissues. qRT-PCR was performed to screen miR-205-5p expression in EC tissues. The roles of miR-205-5p and its candidate target gene, angiopoietin-2 (ANGPT2), in endometriosis progression were confirmed on the basis of both in vitro and in vivo systems. miR-205-5p and ANGPT2 expression were measured by in situ hybridization and immunochemistry, and their clinical significance was statistically analysed.

RESULTS:

miR-205-5p was screened as a novel suppressor of endometriosis through primary ectopic endometrial stromal cell migration, invasion, and apoptosis assay in vitro, along with endometrial-like xenograft growth and apoptosis in vivo. In addition, ANGPT2 was identified as a direct target of miR-205-5p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of ANGPT2 could respectively rescue and simulate the effects induced by miR-205-5p. Importantly, the miR-205-5p-ANGPT2 axis was found to activate the ERK/AKT pathway in endometriosis. Finally, miR-205-5p and ANGPT2 expression were closely correlated with the endometriosis severity.

CONCLUSION:

The newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.

KEYWORDS:

ANGPT2; Endometrial stromal cells; Endometriosis; miR-205-5p

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