Estrogen Regulates the Expression and Function of lncRNA-H19 in Ectopic Endometrium

Songping Liu, Junjun Qiu, Xiaoyan Tang, Qinmei Li, Wei Shao
International journal of women's health · 2022 · vol. Volume 14 , pp. 821–830 · doi:10.2147/ijwh.s365943 · PMID:35789921 · PMC9250333 · W4283588201
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Estrogen upregulates lncRNA-H19 expression in ectopic endometrial stromal cells, which increases their proliferation and invasion, suggesting a role in endometriosis pathogenesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

Liu and colleagues investigated whether estrogen regulates the expression and functional activity of the long noncoding RNA lncRNA-H19 in endometriosis by isolating endometrial stromal cells from ectopic lesions (ecESCs) of 40 confirmed endometriosis patients, comparing them with eutopic and control stromal cells. They measured lncRNA-H19 by RT-PCR and treated ecESCs with 17β-estradiol (10−8 mol/L) for 0–48 hours, then knocked down lncRNA-H19 using lentiviral shRNA to assess proliferation (CCK-8) and invasion (Transwell). lncRNA-H19 was significantly higher in ecESCs than in eutopic and control ESCs, and estrogen increased lncRNA-H19 expression in a time-dependent manner; estrogen-driven increases in proliferation were abolished after lncRNA-H19 knockdown, while estrogen-driven invasion was not altered. The paper does not explicitly state major methodological limitations in the provided text. This paper is centrally about endometriosis—specifically how estrogen regulates lncRNA-H19 expression and affects proliferation and invasion in ectopic endometrial stromal cells.

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Abstract

BACKGROUND: Long noncoding RNAs (lncRNAs) are involved in the pathogenesis of endometriosis and can be regulated by estrogen. This study aimed to investigate the role of estrogen in regulating the expression and function of lncRNA-H19 in endometriosis. METHODS: Endometrial stromal cells (ESCs) were isolated from ectopic, eutopic endometrium with endometriosis and control endometrium without endometriosis, and lncRNA-H19 expression was detected using real-time polymerase chain reaction (RT-PCR). Ectopic endometrial stromal cells (ecESCs) were treated with 17β-estradiol at 10-8mol/L for 0, 12, 24 and 48 hours, and lncRNA-H19 expressions of cells were evaluated using RT-PCR. After ecESCs were treated with 17β-estradiol for 48 hours, lncRNA-H19 expression was knocked down and cell proliferative and invasive abilities were compared. RESULTS: The expression of lncRNA-H19 in ecESCs was significantly higher than that in eutopic endometrial stromal cells (euESCs) and control ESCs. After treated with 17β-estradiol, ecESCshadupregulatedlncRNA-H19 expression with time-dependent manner. Cell proliferation and invasion increased when estrogen upregulated lncRNA-H19 expression in ecESCs, however, cell proliferation restored and cell invasion did not change when lncRNA-H19 was knocked down in ecESCs. CONCLUSION: The expression and function of lncRNA-H19 was regulated by estrogen in ecESCs, which probably contributed to the pathogenesis of endometriosis.

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endometriosis

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