ABSTRACT This study identified miR‐5701 and TP53 through bioinformatics analysis utilizing the GEO, GeneCards, and miRDB databases. The serum expression levels were quantified via Reverse Transcription Quantitative Real‐time Polymerase Chain Reaction (RT‐qPCR). The binding relationship between miR‐5701 and TP53 was confirmed using dual luciferase reporter assays. Subsequently, MC3T3‐E1 cell differentiation was induced with Bone Morphogenetic Protein 2 (BMP2), and the expression changes of miR‐5701 and TP53 after cell differentiation were detected. Subsequently, after overexpression of miR‐5701 and TP53, the expression levels of key osteogenic differentiation markers Alkaline Phosphatase (ALP), Osteocalcin (OCN), and type I collagen were evaluated by ELISA. Serum miR‐5701 expression is downregulated in osteoporotic fracture patients, while it increases after osteoblast differentiation. TP53 is a negative regulatory binding factor downstream of miR‐5701. The mRNA expression of TP53 in the patient serum and the differentiated osteoblast cells is exactly opposite to that of miR‐5701. Overexpression of miR‐5701‐mediated promotion of osteoblast proliferation and differentiation can be reversed by TP53. miR‐5701 was found to facilitate osteoblast proliferation and differentiation through negative regulation of the target gene TP53 expression, suggesting that miR‐5701 could serve as a promising therapeutic target for promoting fracture healing.
Liu et al. (Sun,) studied this question.
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