miR-297 inhibits expression of progesterone receptor and decidualization in eutopic endometria of endometriosis

Tingting Liu, Xiao L, Li Xiao, Pei T, Tianjiao Pei, Bin Luo, Luo B, Tan J, Jing Tan, Ying Long, Long Y, Huang X, Xin Huang, Yunwei Ouyang, Ouyang Y, Wei Huang
Journal of Obstetrics and Gynaecology Research · 2022 · vol. 49(3) , pp. 956–965 · doi:10.1111/jog.15526 · PMID:36572643 · W4312211022
Lab / animal OA: closed CC0 ⤵ 4 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This study found that miR-297 is upregulated in endometriosis endometrial stromal cells, where it represses progesterone receptor expression and inhibits decidualization, contributing to infertility.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

AIM: Progesterone resistance is an epigenetic factor that reduces endometrial receptivity and causes implantation failure in women with endometriosis. In addition, dysregulated miRNAs contribute to the underlying pathogenic mechanisms of endometriosis. This study aimed to determine the effect of miR-297 on the progesterone receptor (PR) expression and on insufficient decidualization of endometrial stromal cells (ESCs) within the eutopic endometria of infertile women with minimal or mild endometriosis. METHODS: ESCs were isolated from infertile endometriosis and normal patients and were transfected with miR-297 mimic or miR-297 inhibitor or respective control. qRT-PCR and western blot were conducted to quantify the expression of miR-297 and PR. The effect of miR-297 on ESCs decidualization was investigated by induced decidualization in vitro. RESULTS: We observed an increase in miR-297 expression and a decrease in the expression of PR in the ESCs from endometriosis patients. Moreover, the expression of PR, most notably PRB, was found to be downregulated following transfection with miR-297 mimic and upregulated following treatment with miR-297 inhibitor. In addition, overexpressed miR-297 inhibited the decidualization of ESCs in vitro. We further determined that miR-297 exerts direct regulatory effects on PR expression. CONCLUSIONS: We demonstrated that miR-297 interferes with fertility by repressing the expression of PR and preventing efficient decidualization in eutopic endometria. Further, miR-297 directly contributes to progesterone resistance in minimal or mild cases of endometriosis. Thus, regulation of miR-297 may prove to be a promising therapeutic strategy for endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (38)

Cited by (4)

Source provenance

europepmc
last seen: 2026-10-12T06:17:10.165071+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-12T06:15:20.425081+00:00
unpaywall
last seen: 2026-10-11T06:28:45.473802+00:00
License: CC0 · commercial use OK