Because of limited treatment options, preeclampsia (PE) is the leading cause of perinatal morbidity and mortality worldwide. Recently, lncRNA TDRG1 is reported to be aberrantly down-regulated in PE placenta, and the abnormal expression of TDRG1 might play a key or partial role in PE development. In this study, we found that TDRG1 was significantly down-regulated in PE placenta compared with the normal placenta.The cell proliferation, migration, invasion, and cell cycle were explored by CCK-8, wound-healing, transwell, and flow cytometer assay, respectively. Experimental results showed that TDRG1 accelerated the proliferation, migration, and invasion of trophoblast cells. Dual-luciferase reporter assays confirmed that TDRG1 could bind to miR-214-5p. Besides, knockdown of TDRG1 suppressed the cell proliferation, migration, and invasion, while knockdown of miR-214-5p reversed the effect. Jagged1 and Notch1 were negatively regulated by miR-214-5p while positively modulated by TDRG1. In conclusion, TDRG1 promoted trophoblast cells viability and invasion by negatively regulating miR-214-5p expression, contributing to a better understanding of PE pathogenesis and providing new light on TDRG1-directed diagnosis and treatment.Significance of the study: In this work, we observed that TDRG1 was able to promote cell proliferation, migration, and invasion cells by suppressing the expression of miR-214-5p and regulating the Notch signalling pathway in trophoblast cells. As far as we know, the effect of TDRG1/miR-214-5p axis on cell viability, migration, and invasion of trophoblast cells was firstly introduced. Our findings provided a better understanding of the mechanism of PE. Moreover, it is reasonable to believe that TDRG1 may be employed as a strategy to treat PE in the future.
K E Y W O R D SmiR-214-5p, Notch1, preeclampsia, TDRG1, trophoblast cells
