Long Non-Coding RNA Prostate Cancer Non-Coding RNA 1/miR-211-5p/Death Effector Domain Containing 2 Axis Affects Preeclampsia by Modulating Trophoblast Cells Proliferation and Apoptosis

Abstract

Background: Preeclampsia (PE) is a pregnancy-specific hypertensive disorder that affects 5–7% of pregnant women and is characterized by edema, hypertension and proteinuria. It is one of the leading causes of morbidity and mortality in pregnant women and newborns. Evidences reveal that the expression of long non-coding RNA (lncRNA) prostate cancer non-coding RNA 1 (PRNCR1) is abnormal in PE. Therefore, we investigated the role of lncRNA PRNCR1 in PE development and its molecular mechanism. Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to determine the expression levels of lncRNA PRNCR1, microRNA (miR)-211-5p and mRNA leval of death effector domain containing 2 (DEDD2). Besides, the expression level of DEDD2 was detected by western blot assay. Cell proliferation ability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, and cell apoptosis was detected by flow cytometry assay. Transwell assay was used to detect the migration and invasion of HTR-8/SVneo cells. The relationship between miR-211-5p and lncRNA PRNCR1 or DEDD2 was verified by dual luciferase reporter gene assay. Results: Over-expression of lncRNA PRNCR1 induced apoptosis, impeded proliferation, migration, invasion in HTR-8/SVneo cells. Knockdown of lncRNA PRNCR1 inhibited apoptosis, promoted cell proliferation, migration and invasion, and all these effects were offset by miR-211-5p inhibitor. The mRNA and protein levels of DEDD2 were decreased by overexpressing miR-211-5p in HTR-8/SVneo cells, while miR-211-5p inhibitor significantly increased the mRNA and protein levels of DEDD2. Conclusions: lncRNA PRNCR1 regulated cell behavior (proliferation, apoptosis, migration, and invasion) via the miR-211-5p/DEDD2 axis in HTR-8/SVneo cells. Thus, lncRNA PRNCR1 participated in the occurrence and development of PE.