Introduction:
The purpose of this research was to investigate whether lncRNA SNHG6 has an effect on the pathogenesis of gestational diabetes mellitus (GDM).

Material and methods:
Placental tissue was collected from patients with GDM and from pregnant women without GDM. Expression of lncRNA SNHG6 and EZH2 in the placental tissue was detected by qRT-PCR, immunohistochemistry (IHC), and western blotting. An in vitro cell model for GDM using high-dose glucose was employed to measure relative expression of mRNA and proteins by RT-qPCR and WB assay, and cell viability, apoptosis rate, invasion cell number, and wound healing rate by CCK-8, flow cytometry, transwell assay, and wound healing assay, respectively. Correlation between miRNA-26a-5p and EZH2 was investigated with a dual-luciferase reporter assay.

Results:
Compared with the control placenta, lncRNA SNHG6 and EZH2 mRNA expression levels were significantly depressed and EZH2 protein expression was significantly downregulated in GDM placenta tissues (p < 0.001, respectively). In the in vitro cell model, lncRNA SNHG6 overexpression significantly improved high-dose glucose-induced HTR-8/SVneo cell function losses, including proliferation, migration, and invasion, by significantly depressing miRNA-26a-5p via regulation of EZH2 expression. The dual-luciferase reporter assay revealed that miRNA-26a-5p could target to EZH2 in HTR-8/SVneo cells.

Conclusions:
Expression of lncRNA SNHG6 in the placenta of patients with GDM is abnormally decreased. Overexpression of lncRNA SNHG6 improved HTR-8/SVneo cell function via regulation of the miRNA-26a-5p/EZH2-H3K27me3 pathway in an in vitro GDM model.