MicroRNA-766-3p modulates the progression of delayed fracture healing by targeting TGFBR1

Objectives A certain number of patients frequently encounter delayed fracture healing (DFH) following surgery. This study intended to investigate the functionality of miR-766-3p in the progression of DFH. Methods The research encompassed 100 normal tibial fracture healing patients and 95 DFH patients. RT-qPCR was implemented to measure the expression, and the ROC was used to determine the diagnostic value of miR-766-3p for DFH patients. Cox regression was performed to identify the independent risk factors associated with DFH. Moreover, we further analyzed the regulatory effects of miR-766-3p and TGFBR1 on osteogenic markers. The CCK-8 method and flow cytometry were utilized to detect proliferation and apoptosis. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were quantified using enzyme-linked immunosorbent assay (ELISA). The dual-luciferase reporter gene assay was carried out to detect the targeted relationship. Results In DFH patients, miR-766-3p exhibited a downward movement. miR-766-3p served as an independent prognostic factor influencing DFH. miR-766-3p increased after the induction and differentiation of MC3T3-E1 cells. Elevated miR-766-3p could enhance the expression of osteogenic markers, facilitate proliferation and differentiation, inhibit inflammatory reactions, and reduce apoptosis. Additionally, when TGFBR1 was upregulated, it reversed the effect of miR-766-3p on osteoblasts. miR-766-3p may emerge as a feasible predictive biomarker for patients with DFH. Conclusions miR-766-3p exerted its regulatory function on DFH by targeting TGFBR1 .