Expression and role of miR‑338‑3p in peripheral blood and placenta of patients with pregnancy‑induced hypertension
Affiliations: Fetal Heart Monitoring Unit, Laiwu Maternal and Child Health Hospital, Laiwu, Shandong 271100, P.R. China, The Fifth Department of Obstetrics and Gynecology, Laiwu Maternal and Child Health Hospital, Laiwu, Shandong 271100, P.R. China
- Published online on: May 6, 2020 https://doi.org/10.3892/etm.2020.8719
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The present study aimed to investigate the role of miR-338-3p in pregnancy-induced hypertension (PIH), and its effects on human trophoblast cells in vitro. Quantitative real‑time PCR was used to detect miR‑338‑3p expression. Human trophoblast HTR8/SVneo cells were transfected with miR‑338‑3p mimics. Effects of miR‑338‑3p on cell proliferation, invasion and metastasis, and anoikis resistance were detected by CCK‑8 assay, Transwell chamber assay, flow cytometry and western blot analysis, respectively. Bioinformatics analysis was performed to predict the target of miR‑338‑3p, and the results were confirmed by dual luciferase reporter assay. The expression level of miR‑338‑3p was significantly upregulated in the peripheral blood and placenta of PIH patients. CCK‑8 assay showed that miR‑338‑3p mimics inhibited the proliferation of HTR8/SVneo cells at indicated time points. Flow cytometry showed that miR‑338‑3p transfection significantly increased the Ki‑67 expression in the HTR8/SVneo cells, indicating enhanced cell proliferation. Transwell chamber assay and western blot analysis showed that the invasion and metastatic abilities of the HTR8/SVneo cells were significantly decreased in the miR‑338‑3p transfection group, as well as expression levels of MMP‑2 and MMP‑9. Bioinformatics analysis and dual luciferase reporter assay indicated that AKT3 is a target gene of miR‑338‑3p. Our results suggest that miR‑338‑3p is significantly increased in the peripheral blood and placenta of PIH patients, which is correlated with the disease development. miR‑338‑3p inhibits proliferation, invasion and metastasis, and apoptosis resistance of human trophoblast cells by targeting AKT3.