Folia Biologica
Journal of Cellular and Molecular Biology, Charles University 

Delayed fracture healing (DFH) poses a considerable challenge in the clinical treatment of fractures, imposing substantial negative impacts on patients. This study intends to determine the diagnostic significance of miR-339-3p in DFH and further analyses its molecular mechanism in osteoblast differentiation. A total of 98 patients with DFH and 106 patients with normal fracture healing provided serum samples and baseline data for this study. The impact and diagnostic value of miR-339-3p in DFH were respectively assessed via logistic regression analysis and ROC curve. Employing MC3T3-E1 as the model cells for osteogenic differentiation, cell experiments were carried out. The expression levels of insulin-like growth factor 2, miR-339-3p and osteogenic differentiation markers were detected using the RT-qPCR method and Western blot assays. Cell viability and apoptosis were examined using the CCK8 assay and flow cytometry. The target genes of miR-339-3p were verified through dual-luciferase reporter assays. In patients with DFH, the expression of miR-339-3p was up-regulated, whereas the expression level of IGF2 was down-regulated. miR-339-3p served as a potential biomarker for DFH and exhibited a negative correlation with IGF2. IGF2 was identified as the target of miR-339-3p. Inhibition of miR-339-3p could up-regulate IGF2 expression, enhance the activity and differentiation of MC3T3-E1 cells, and suppress their apoptosis. Promoting miR-339-3p exerted the opposite effect. On this foundation, an increase in IGF2 could reverse this tendency. miR-339-3p demonstrates diagnostic potential for DFH. Inhibiting the expression of miR-339-3p can enhance cell activity and osteogenic differentiation through negative regulation of IGF2, thus suppressing the onset of DFH.

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