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Background <p>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.</p> Methods <p>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.</p> Results <p>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.</p> Conclusions <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Ruiping Yu,
  • Xiaoyan Liu,
  • Sai Zhang

摘要

Background

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.

Methods

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.

Results

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.

Conclusions

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.