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Gestational diabetes mellitus (GDM) is a common metabolic condition during pregnancy. Long non-coding RNAs (lncRNAs) have been found to seve critical roles in GDM development; however, the role of lncRNA maternally expressed gene 3 (MEG3) in GDM remains unclear. Therefore, the aim of the present study was to investigate the expression and role of MEG3 in GDM, and to further explore the underlying mechanism. The levels of lncRNA MEG3 in the blood and placental villous tissues of pregnant women with GDM was measured using reverse transcription-quantitative PCR. Bioinformatics analysis and dual luciferase reporter assays were performed to investigate the association between lncRNA MEG3 and microRNA (miR)-345-3p. Transfection was subsequently performed on HTR-8/SVneo cells, a human chorionic trophoblast cell line, to assess the role of lncRNA MEG3 in GDM. In particular, cell viability, cellular migratory/invasive ability and cell apoptosis were analyzed using MTT assay, Transwell assay and flow cytometry, respectively. Compared with pregnant women without GDM, lncRNA MEG3 levels were significantly elevated in the blood and placental villous tissues of GDM pregnant women. miR-345-3p was identified to be a direct target of lncRNA MEG3 using dual luciferase reporter assay, which was found to be reduced in pregnant women with GDM. Further analysis demonstrated that lncRNA MEG3 overexpression significantly inhibited HTR-8/SVneo cell viability, and prevented cell migration and invasion in addition to inducing cell apoptosis. In contrast, lncRNA MEG3 knockdown significantly enhanced HTR-8/SVneo cell viability, promoted cell migration/invasion and reduced cell apoptosis. Inhibiting miR-345-3p expression negated all the observed physiological effects of lncRNA MEG3 knockdown on HTR-8/SVneo cells. In conclusion, lncRNA MEG3 levels were abnormally upregulated in GDM, which participated in the development and progression of GDM by regulating human chorionic trophoblast cell physiology. Therefore, lncRNA MEG3 may be a potential diagnostic and therapeutic target for GDM.

Mechanism associated with aberrant lncRNA MEG3 expression in gestational diabetes mellitus