دورية أكاديمية

PCGEM1 promotes cell proliferation and migration in endometriosis by targeting miR-124-3p-mediated ANTXR2 expression

التفاصيل البيبلوغرافية
العنوان: PCGEM1 promotes cell proliferation and migration in endometriosis by targeting miR-124-3p-mediated ANTXR2 expression
المؤلفون: Yong Liu, Chengmao Xie, Ting Li, Chang Lu, Linyuan Fan, Zhan Zhang, Sha Peng, Na Lv, Dan Lu
المصدر: BMC Women's Health, Vol 23, Iss 1, Pp 1-9 (2023)
بيانات النشر: BMC, 2023.
سنة النشر: 2023
المجموعة: LCC:Gynecology and obstetrics
LCC:Public aspects of medicine
مصطلحات موضوعية: PCGEM1, miR-124-3p, ANTXR2, Endometriosis, Cell proliferation, Cell migration, Gynecology and obstetrics, RG1-991, Public aspects of medicine, RA1-1270
الوصف: Abstract Background Endometriosis, a common gynaecological disease in women, affects 10% of women of childbearing age. Among infertile women, this proportion is as high as 30–50%. Despite the high prevalence of endometriosis, the pathogenesis of endometriosis is still unclear. Methods In the present study, bioinformatics analysis and molecular and animal experiments were employed to explore the functions of PCGEM1 in the pathogenesis of endometriosis. We established an endometriosis rat model and isolated endometrial stromal cells (ESCs) and primary normal ESCs (NESCs). Bioinformatics analysis was adopted to study the roles of PCGEM1 in promoting the pathogenesis of endometriosis. Luciferase reporter assays and RNA pull-down assays were carried out to study the mechanism by which PCGEM1 regulates ANTXR2. Results Our results indicated that PCGEM1 promoted the motility and proliferation of ectopic endometrial cells, and the underlying mechanism was due to the direct binding of PCGEM1 to miR-124-3p to modulate ANTXR2 expression. Conclusion PCGEM1 can influence endometrial stromal cell proliferation and motility and may be a novel therapeutic target for endometriosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1472-6874
Relation: https://doaj.org/toc/1472-6874
DOI: 10.1186/s12905-023-02250-1
URL الوصول: https://doaj.org/article/1457bac019084c0484cb21fb3475fc32
رقم الأكسشن: edsdoj.1457bac019084c0484cb21fb3475fc32
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14726874
DOI:10.1186/s12905-023-02250-1