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miR-345-3p serves a protective role during gestational diabetes mellitus by targeting BAK1
1Department of Gynecology and Obstetrics, Wuhan Children's Hospital, Wuhan Maternal and Child Healthcare Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430010, P.R. China.
Recent studies have demonstrated that microRNAs (miRs) serve a crucial role during the development of gestational diabetes mellitus (GDM). However, the mechanisms underlying miR-345-3p and its protective role during GDM have not been previously reported. The present study investigated miR-345-3p expression and function in vitro, and the possible molecular mechanisms underlying GDM. Compared with healthy pregnant women, miR-345-3p was downregulated in the placental tissue and peripheral blood of patients with GDM. Further investigation revealed that BCL2-antagonist/killer 1 (BAK1) was a predicted target gene of miR-345-3p, and the expression of BAK1 was significantly increased in patients with GDM compared with healthy pregnant women. In vitro analysis revealed that miR-345-3p mimic significantly increased cell viability, migration and invasion, inhibited apoptosis, upregulated Bcl-2 and matrix metallopeptidase 9 expression, and decreased Bax expression compared with the control group. Furthermore, miR-245-3p mimic-induced alterations were reversed by BAK1 overexpression. The results suggested that miR-345-3p overexpression exhibited a protective role in patients with GDM by inhibiting HTR8-/SVneo cell apoptosis, and promoting cell proliferation and migration via targeting BAK1. The use of miR-345-3p for the diagnosis of GDM requires further investigation.
Recent studies have demonstrated that microRNAs (miRs) serve a crucial role during the development of gestational diabetes mellitus (GDM). However, the mechanisms underlying miR-345-3p and its protective role during GDM have not been previously reported. The present study investigated miR-345-3p expression and function in vitro, and the possible molecular mechanisms underlying GDM. Compared with healthy pregnant women, miR-345-3p was downregulated in the placental tissue and peripheral blood of patients with GDM. Further investigation revealed that BCL2-antagonist/killer 1 (BAK1) was a predicted target gene of miR-345-3p, and the expression of BAK1 was significantly increased in patients with GDM compared with healthy pregnant women. In vitro analysis revealed that miR-345-3p mimic significantly increased cell viability, migration and invasion, inhibited apoptosis, upregulated Bcl-2 and matrix metallopeptidase 9 expression, and decreased Bax expression compared with the control group. Furthermore, miR-245-3p mimic-induced alterations were reversed by BAK1 overexpression. The results suggested that miR-345-3p overexpression exhibited a protective role in patients with GDM by inhibiting HTR8-/SVneo cell apoptosis, and promoting cell proliferation and migration via targeting BAK1. The use of miR-345-3p for the diagnosis of GDM requires further investigation.
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