Expression and function of lncRNA MALAT1 in gestational diabetes mellitus

Background: Gestational diabetes mellitus (GDM) severely threatens maternal and fetal health. Long non-coding RNA (lncRNA) participates in the regulation of various cellular processes. Objectives: Previous studies have identified the role of lncRNA MALAT1 in diabetic retinopathy-related inflammation. However, the role of lncRNA MALAT1 in GDM has not been reported yet. Material and methods: Real-time polymerase chain reaction (RT-PCR) was used to measure the lncRNA MALAT1 expression level in placental tissues from GDM patients and from a normal pregnant group. Placental trophoblastic-derived cell line HTR8 cells were divided into a control group, an siRNA negative control group and a MALAT1 siRNA group. The cells underwent RT-PCR analysis of lncRNA MALAT1 expression, an MTT assay of cell proliferation, and a transwell assay of cell invasion and migration. In addition, enzyme-linked immunosorbent assay (ELISA) was used to analyze the level of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). Western blotting was used to measure the changes of the tumor growth factor beta (TGF-beta)/nuclear factor-kappa B (NF-kappa B) signaling pathway. Results: Gestational diabetes mellitus placental tissues showed higher lncRNA MALAT1 expression compared to a normal control group (p < 0.05). After siRNA intervention, lncRNA MALAT1 showed decreased expression in the trophoblastic layer; inhibited trophoblastic cell proliferation, migration, or invasion; decreased the secretion of inflammatory factors TNF-alpha and IL-6; and suppressed the expression of TGF-beta and NF-kappa B compared to that of the control and siRNA-NC groups (p < 0.05). Conclusions: Gestational diabetes mellitus appears to upregulate lncRNA MALAT1. Downregulation of lncRNA MALAT1 inhibits inflammation and suppresses the proliferation, invasion and migration of GDM placental trophoblastic cells, possibly by modulating the TGF-beta/NF-kappa B signaling pathway.