Identification of serum miR‑320a in gestational diabetes mellitus for predicting macrosomia and in vitro mechanistic investigation

Gestational diabetes mellitus (GDM) significantly elevates the risk for a spectrum of adverse pregnancy outcomes. The expression pattern and regulatory mechanism of microRNA-320a (miR-320a) in GDM remain poorly elucidated. The study enrolled 40 GDM patients along with 40 healthy controls. Serum expression levels of miR-320a were quantified using reverse transcription quantitative polymerase chain reaction (RT-qPCR). ROC curve analysis and binary logistic regression were applied to evaluate its diagnostic performance for GDM and predictive value for fetal macrosomia, respectively. In HTR-8/SVneo trophoblast cells, CCK-8 assay and flow cytometry were used to assess the influence of miR-320a on cell proliferation and apoptosis. Dual-luciferase reporter assay validated the direct targeting relationship between miR-320a and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta (PIK3CD). Western blot was performed to detect PIK3CD protein expression, and rescue experiments further explored the biological function of the miR-320a/PIK3CD axis in trophoblast proliferation and apoptosis. Serum miR-320a was significantly downregulated in GDM patients and exhibited good diagnostic capability to distinguish GDM from healthy pregnancies. Lower miR-320a expression was correlated with a higher risk of fetal macrosomia. In addition, overexpression of miR-320a promoted cell proliferation and suppressed apoptosis in HTR‑8/SVneo cells. PIK3CD was identified as a direct downstream target of miR‑320a, and miR‑320a overexpression inhibited PIK3CD expression. Furthermore, the effects of miR‑320a on cell proliferation and apoptosis were markedly reversed by co‑transfection with pcDNA‑PIK3CD. Circulating miR-320a has promising potential for GDM diagnosis and fetal macrosomia prediction. Increased miR-320a expression facilitates proliferation and restricts apoptosis in HTR-8/SVneo trophoblast cells by directly targeting PIK3CD.