miR-1290 serves as a potential biomarker for osteoporotic fracture and regulates osteoblast function by targeting KDM5A.

Abstract

This study aims to investigate the expression characteristics, clinical diagnostic value of miR-1290 in osteoporotic fracture (OPF) patients, and its regulatory mechanism in osteoblast function. 289 subjects were divided into healthy control, OP, and OPF groups. Serum miR-1290 levels were detected by RT-qPCR, and its diagnostic efficacy was evaluated via ROC curve analysis. Functional experiments were conducted using hFOB1.19 cells to explore miR-1290's expression pattern during osteogenic differentiation and its effects on cell proliferation and differentiation. Bioinformatics prediction, dual-luciferase reporter assay, and RIP assay were used to verify the target gene of miR-1290. Serum miR-1290 levels showed a gradient decrease from healthy controls to OP and OPF patients. It had favorable diagnostic efficacy for distinguishing OPF from OP patients. OPF patients' postoperative miR-1290 levels gradually increased. miR-1290 was upregulated during osteogenic differentiation and promoted osteoblast proliferation and differentiation. KDM5A was identified as a direct target of miR-1290, and their expressions were negatively correlated. KDM5A overexpression reversed miR-1290's enhancement of osteoblast proliferation and differentiation. miR-1290 is downregulated in OP and OPF patients and promotes osteoblast function by targeting KDM5A, which highlights the role of the miR-1290/KDM5A axis in OPF and offers new insights for clinical diagnosis and targeted therapy.