LncRNA H19 is downregulated in ectopic endometrial stromal cell by multiple medicines in vitro
Objective: According to the previous studies, it has been found that long non-coding RNA H19 (lncRNA H19)-ITGB3-miR-124-3p axis can regulate cell proliferation and invasion of the ectopic endometrium, which could be the potential pathway for treating endometriosis by a key medicine. The aim of this study was to investigate the roles of metformin, aspirin, artemisinin, and berberine in regulating the expression of lncRNA H19 in ectopic endometrial stromal cells (ecESCs) and explore novel medicines for the treatment of endometriosis. Methods: Isolation of ESCs from the ectopic endometrium of patients with endometriosis and treatment with metformin at 0.1 mmol/L, aspirin at 5.00 mmol/L, artemisinin at 20 μmol/L, and berberine at 20 μmol/L for 0, 12, 24, and 48 hours. LncRNA H19 levels in ecESCs after treatment were evaluated using real-time polymerase chain reaction, and changes in cell proliferation and invasion were determined using Cell Counting Kit-8 and Transwell assays. Results: lncRNA H19 levels in ecESCs in the metformin, aspirin, artemisinin, and berberine groups were significantly lower than those in the control group, with inhibition of cell proliferation and invasion; metformin and berberine showed the highest efficiency. Conclusions: Metformin and berberine inhibited ecESC proliferation and invasion by downregulating lncRNA-H19 levels, offering a novel treatment for endometriosis.
Authors
- Songping Liu (ORCID: https://orcid.org/0000-0002-6561-3049)
- Xiaoxiao Gao (ORCID: https://orcid.org/0000-0002-3153-9370)
- Wei Shao (ORCID: https://orcid.org/0000-0003-1126-5939)
- Jiaqi Wang (ORCID: https://orcid.org/0000-0001-8841-0124)
- Han Gao (ORCID: https://orcid.org/0009-0001-6603-8322)
Institutions
- Jinshan Hospital of Fudan University (CN)
Publication Details
- Journal
- Reproductive and Developmental Medicine
- Published
- 2024-12-11
- DOI
- https://doi.org/10.1097/rd9.0000000000000119
- Citations
- 2
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.57