ArticleJournal of orthopaedic surgery and research2025
The mechanism of lncRNA LINC01446 in delayed fracture healing and its clinical significance.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLong non-coding RNAs (lncRNAs) exert a vital role in the fracture healing process by interacting with microRNAs (miRNAs) and constructing lncRNA-miRNA regulatory networks. This study focuses on clarifying lncRNA LINC01446's role in delayed fracture healing (DFH) and exploring its potential regulatory mechanism.
methodsThe expression of LINC01446 and miR-338-3p in serum samples was detected via qRT-PCR, and the predictive ability of LINC01446 for DFH in fracture patients was evaluated by the ROC curve. The targeting interaction between LINC01446 and miR-338-3p was predicted via StarBase and confirmed through the dual-luciferase reporter assay. For the assessment of cell proliferation and apoptosis, the CCK-8 assay and flow cytometry were utilized.
resultsIn DFH, LINC01446 was significantly downregulated, while miR-338-3p was notably increased. The relationship between LINC01446 and miR-338-3p was identified, showing an inverse regulatory pattern. Knockdown of LINC01446 lowered osteogenic marker gene expression, inhibited the proliferation of MC3T3-E1 cells, and induced cell apoptosis. Additionally, the miR-338-3p inhibitor effectively abrogated the suppressive effects of LINC01446 knockdown on osteoblastic proliferation and differentiation, as well as its promotional effect on cell apoptosis (P < 0.05).
conclusionsLINC01446 can affect DFH via miR-338-3p and may act as a potential therapeutic target.
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