文献类型：期刊文献

英文题名：Silencing of circ_0007299 suppresses proliferation, migration, and invasiveness and promotes apoptosis of ectopic endometrial stromal cells in endometriosis via miR-424-5p-dependent modulation of CREB1

作者：Mao, Haiyan[1,2];Zhang, Xiaohua[1];Yin, Lu[3];Ji, Xiujia[1];Huang, Cancan[1];Wu, Quansheng[1]

第一作者：Mao, Haiyan

通信作者：Wu, QS[1]

机构：[1]Gansu Univ Tradit Chinese Med, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Prov Hosp, Tradit Med Diag & Treatment Ctr, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China;[3]Lanzhou Univ Second Hosp, Lanzhou, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Tradit Chinese Med, 35 Dingxi East Rd, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2023

卷号：307

期号：1

起止页码：149

外文期刊名：ARCHIVES OF GYNECOLOGY AND OBSTETRICS

收录：;Scopus(收录号：2-s2.0-85132116030);WOS:【SCI-EXPANDED(收录号:WOS:000812034200003)】；

基金：The present study was supported by National Natural Science Fund Regional Foundation Project (No. 81760879).

语种：英文

外文关键词：Endometrial stromal cells (ESCs); Endometriosis; circ_0007299; miR-424-5p; CREB1

摘要：Background The abnormality of endometrial stromal cells (ESCs) can contribute to endometriosis pathogenesis. Circular RNAs (circRNAs) possess critical roles in endometriosis pathogenesis. Here, we defined the activity and mechanism of human circ_0007299 in the regulation of ectopic ESCs in vitro. Methods Circ_0007299, miR-424-5p and cAMP response element-binding protein 1 (CREB1) were quantified by qRT-PCR or immunoblotting. Cell viability, proliferation, apoptosis, invasion and motility were gauged by CCK-8, 5-Ethynyl-2MODIFIER LETTER PRIME-Deoxyuridine (EdU), flow cytometry, transwell, and wound-healing assays, respectively. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to verify the direct relationship between miR-424-5p and circ_0007299 or CREB1. Results Our data showed that circ_0007299 was upregulated in human ectopic endometrium tissues and ectopic ESCs. Silencing endogenous circ_0007299 impeded the proliferation, invasiveness, and motility and enhanced apoptosis of ectopic ESCs. Mechanistically, circ_0007299 regulated miR-424-5p expression. Moreover, circ_0007299 silencing impeded the proliferation, invasiveness, and motility and enhanced apoptosis of ectopic ESCs via its regulation on miR-424-5p. CREB1 was identified as a direct miR-424-5p target, and miR-424-5p overexpression suppressed ectopic ESC proliferation, migration, and invasiveness and promoted apoptosis by downregulating CREB1. Furthermore, circ_0007299 positively modulated CREB1 expression through miR-424-5p competition. Conclusion Our findings establish that circ_0007299 silencing impedes the proliferation, invasiveness, and motility and promotes apoptosis of ectopic ESCs at least in part via miR-424-5p-dependent modulation of CREB1.