MicroRNA‑1323 serves as a biomarker in gestational diabetes mellitus and aggravates high glucose‑induced inhibition of trophoblast cell viability by suppressing TP53INP1

Abstract

Gestational diabetes mellitus (GDM) leads to poor pregnancy outcomes, and microRNAs (miRNAs/miRs) have been suggested to be associated with GDM, but the pathological mechanisms remain unclear. The present study aimed to investigate the diagnostic value of miR-1323 in GDM patients and its effects on trophoblast cell viability. Additionally, the present study investigated the correlation between miR-1323 and TP53INP1 to understand the pathological mechanism of GDM progression. Reverse transcription-quantitative polymerase chain reaction was used to detect the miR-1323 expression and TP53INP1 mRNA expression. The diagnostic value of serum miR-1323 was evaluated by receiver operating characteristic analysis. HTR-8/SVneo and BeWo cells were treated with high glucose (HG) to construct cell models of GDM, and trophoblast cell viability was assessed using an MTT assay. The protein expression of TP53INP1 was detected by western blot analysis. The correlation between miR-1323 and TP53INP1 was investigated by luciferase reporter assay. The miR-1323 expression was increased in patients with GDM, which had relatively high diagnostic accuracy for GDM screening and was positively correlated with fasting blood glucose in patients GDM. HG upregulated the miR-1323 expression and inhibited trophoblast cell viability. Overexpression of miR-1323 significantly inhibited the viability of HG-induced trophoblast cells. TP53INP1, a target gene of miR-1323, was negatively correlated with miR-1323. TP53INP1 overexpression reversed the inhibitory effect of miR-1323 overexpression on the viability of HG-treated trophoblast cells. Increased levels of serum miR-1323 may be a diagnostic biomarker for GDM. Additionally, miR-1323 may inhibit trophoblast cell viability by inhibiting TP53INP1, suggesting that it may be a potential therapeutic target for GDM.