Hsa_circ_0001740 mediates trophoblast cell function via regulating miR‐188‐3p/ARRDC3

Abstract

AbstractPreeclampsia is an obstetric disorder and remains the leading contributor to maternal and fetal morbidity and mortality. This study was designed to explore the role of hsa_circ_0001740 in preeclampsia as well as its underlying mechanism. Real‐time quantitative polymerase chain reaction was performed to examine hsa_circ_0001740 and miR‐188‐3p levels in trophoblast cell line HTR‐8/SVneo. The proliferation, migration, invasion, and apoptosis of HTR‐8/SVneo cells were detected using cell counting kit‐8, colony formation, wound healing, transwell, and terminal‐deoxynucleoitidyl transferase mediated nick end labeling assays, respectively. The expression of apoptosis‐ and Hippo signaling‐related proteins were assessed by western blot. Moreover, the binding relationship between hsa_circ_0001740 and miR‐188‐3p, miR‐188‐3p and ARRDC3 were verified by luciferase report assay. The results showed that hsa_circ_001740 overexpression inhibited the proliferation, migration, and invasion, and promoted apoptosis of HTR‐8/SVneo cells. Hsa_circ_0001740 was verified to bind to miR‐188‐3p, and ARRDC3 was demonstrated to be a target of miR‐188‐3p. miR‐188‐3p overexpression partially counteracted the suppressive effects of hsa_circ_001740 overexpression on the proliferation, migration, and invasion of HTR‐8/SVneo cells. What's more, ARRDC3 expression was upregulated by hsa_circ_001740‐overexpression but was downregulated by miR‐188‐3p overexpression. Hsa_circ_001740/miR‐188‐3p also mediated Hippo signaling. To summarize, hsa_circ_0001740 could maintain trophoblast cell function via downregulating miR‐188‐3p, providing a potential biomarker for the diagnosis and treatment of preeclampsia.