Clinical significance of lncRNA EGFR-AS1 in gestational diabetes mellitus and its regulation of endothelial cell function.

Authors

Hui Jiang, Pengcheng Wu, Min Zhang, Congxiang Liu

Published in

Irish journal of medical science. Jun 24, 2026. Epub Jun 24, 2026.

Abstract

Gestational diabetes mellitus (GDM) causes APOs. The diagnostic OGTT has a lag, and the role of lncRNA EGFR-AS1 in GDM has potential.
This study evaluated the potential of EGFR-AS1 for the GDM clinical application and explored the role of the EGFR-AS1/miR-142-5p/ROCK2 axis in placental endothelial injury.
Serum EGFR-AS1, miR-142-5p and ROCK2 levels were detected via qPCR in 135 GDM patients and 110 healthy pregnant women. The clinic value of EGFR-AS1 was analyzed using ROC and logistic regression. A high glucose (HG)-induced model was established, in which EGFR-AS1 was silenced alone or co-silenced with miR-142-5p. The regulatory mechanism of EGFR-AS1/miR-142-5p/ROCK2 axis on placental endothelial injury was then analyzed via CCK-8, ELISA, qPCR, and WB.
In GDM patients, serum EGFR-AS1 and ROCK2 were elevated, whereas miR-142-5p was reduced. Serum EGFR-AS1 showed high diagnostic efficiency for GDM and acted as an independent predictor of APOs occurrence. Silencing EGFR-AS1 reversed HG-induced HPVECs injury-evidenced by inhibited inflammatory factor release, balanced oxidative stress, up-regulated pro-angiogenic factors mRNA expression, and down-regulated proteins expression related to apoptosis and endothelial injury. Dual-luciferase reporter assays confirmed binding between EGFR-AS1 and miR-142-5p, as well as between miR-142-5p and ROCK2. Notably, co-inhibiting EGFR-AS1 and miR-142-5p abolished the protective effect of EGFR-AS1 silencing.
EGFR-AS1 is a clinical auxiliary biomarker for GDM diagnosis and prediction. It aggravates HPVECs injury via EGFR-AS1/miR-142-5p/ROCK2 axis, which impairs placental function and triggers APOs, providing a new target for GDM intervention.

PMID:
42340571
Bibliographic data and abstract were imported from PubMed on 24 Jun 2026.

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