Reprod Biol. 2024 Mar 7;24(2):100876.doi: 10.1016/j.repbio.2024.100876. Online ahead of print.

Circ_0001495 influences the development of endometriosis through the miRNA-34c-5p/E2F3 axis

Affiliations

Affiliations

  • 1 Anhui Medical University, Hefei, Anhui 230032, China; Department of Gynaecology, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241000, China; Department of Gynaecology, The First People’s Hospital of Wuhu, Wuhu, Anhui 241000, China.
  • 2 Department of Gynaecology, The First People’s Hospital of Wuhu, Wuhu, Anhui 241000, China.
  • 3 Anhui Medical University, Hefei, Anhui 230032, China; Department of Gynaecology, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241000, China. Electronic address: niguantai@wnmc.edu.cn.

Free article

Abstract

Endometriosis is a chronic gynecological condition characterized by the presence of endometrial glands and stroma outside the uterine cavity., accounting for 7% of all female malignant tumors and 20%- 30% of malignant tumors of the female reproductive system. Multiple studies have shown that circular RNA (circRNA) has the potential to become a targeted target and marker for EM. However, the roles of circ_0001495 in EM are still unclear. Our research aims to reveal the molecular mechanism of circ_0001495 in EM. In this study, RT-PCR or western blot were conducted to determine mRNA and protein expression. cell viability, proliferation, migration, invasion, and apoptosis were assessed by CCK-8, EdU, wound healing, transwell, and flow cytometry analyses, respectively. Additionally, the targeting relationship between miR-34c-5p and circ_0001495 or E2F3 was confirmed through dual-luciferase reporter gene assay. We found significant overexpression of circ_0001495 in EM tissues and cells. Knockdown of circ_0001495 inhibited the proliferation, migration and invasion of ectopic endometrial stromal cells (EESCs) and increased cell apoptosis. Moreover, we found that circ_0001495 regulated E2F3 levels by interacting with miR-34c-5p in EESC. Furthermore, in vitro, miR-34c-5p inhibition or E2F3 overexpression could attenuate the effect of circ_0001495 silencing on EM progression. In addition, the vivo experiment demonstrated that inhibition of circ_0001495 could repress the development of endometriosis by regulating the miR-34c-5p/E2F3 axis. In conclusion, our study suggested that circ_0001495 promoted EM progression in vitro and in vivo through the miR-34c-5p/E2F3 axis, which might be a potential therapeutic target for EM.

Keywords: Circ_0001495; E2F3; Endometriosis; MiRNA-34c-5p.

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