Circ_0008927 Promotes the Progression of Endometriosis via miR-608-/PROM2-Mediated Ferroptosis

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AI-generated summary by gemini-2.5-flash-lite, 2026-06-09

Circ_0008927 promotes endometriosis progression by competitively binding miR-608, upregulating PROM2, and inhibiting ferroptosis in endometriosis cells.

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Abstract

OBJECTIVE: Abnormal expression of circular RNA (circRNA) leads to the occurrence and development of endometriosis (EM), but its underlying mechanisms are largely unknown. METHODS: Abnormally expressed circRNAs were screened in EM and normal tissues. A series of gain-of-function or loss-of-function experiments were conducted to evaluate the biological behavior of circ_0008927 in EM cells. The role of circ_0008927 in the proliferation, migration, and invasion of EM cells was investigated. The downstream mechanisms of circ_0008927 were studied through bioinformatics analysis and RNA sequencing, and this was confirmed through RNA immunoprecipitation and dual-luciferase reporter assays. RESULTS: Circ_0008927 is highly expressed in EM tissues. From a biological perspective, silencing circ_0008927 can inhibit the proliferation, migration, and invasion of EMS cells in vitro. Mechanistically, circ_0008927 can interact with miR-608 through a competitive endogenous RNA mechanism, upregulating prominin2 (PROM2) and inhibiting ferroptosis in EM, thereby exacerbating the progression of EM. CONCLUSIONS: Our research results not only reveal the key role of circ_0008927 in regulating the progression of EM but also advocate for attenuating the circ_0008927/miR-608/PROM2 regulatory axis to combat EM.

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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

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References (32)

Source provenance

europepmc
last seen: 2026-08-20T06:14:21.026120+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-08-20T06:11:36.075764+00:00
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