Circ_0008927 promotes the progression of endometriosis via miR-608/PROM2 mediated ferroptosis.

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.