Role and diagnostic value of miR-3188 targeting OGT in regulating osteoblast function in delayed fracture healing of tibial fractures

Abstract

This study investigated the role and mechanism of miR-3188 in delayed healing of tibial fractures, aiming to aid diagnosis and targeted intervention. A total of 172 patients with tibial fracture were enrolled and divided into normal fracture healing group (NFH, n = 82) and DFH ( n = 90). Serum miR-3188 was measured by RT-qPCR, with diagnostic performance evaluated by ROC and logistic regression. Osteogenic markers were measured after inducing differentiation of hFOB 1.19 cells. Predicted downstream targets of miR-3188 were validated by dual-luciferase reporter assay. Cell proliferation and apoptosis were assessed by CCK‑8 and flow cytometry, respectively. Serum miR-3188 levels were significantly elevated in patients with DFH and showed good diagnostic value for distinguishing DFH from NFH (AUC = 0.917, sensitivity 83.33%, specificity 87.80%). miR-3188 was identified as an independent risk factor for DFH (OR = 3.283). Overexpressing miR-3188 impaired proliferation, triggered apoptosis, and lowered mRNA expression of RUNX2, OCN, OPN, along with ALP activity. OGT was confirmed as a direct target of miR-3188 and was negatively regulated by miR-3188, with serum OGT levels negatively correlated with miR-3188 ( r = − 0.717). OGT overexpression partially alleviated the inhibition of osteoblast function caused by miR-3188 mimic. miR-3188 may serve as a potential diagnostic biomarker for DFH. The miR-3188/OGT axis participates in fracture healing by regulating osteoblast function, and miR-3188 represents a promising new target for the treatment of DFH.