Song Zhou, ZeWen Zheng, ChuanKai Zhang, Liang Hao, Qiang Chen, Ke Sun, Min Cai
{"title":"LncRNA linc01123通过miR-134-5p/XIAP轴介导骨折愈合受损。","authors":"Song Zhou, ZeWen Zheng, ChuanKai Zhang, Liang Hao, Qiang Chen, Ke Sun, Min Cai","doi":"10.1186/s13018-025-06167-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The prolonged recovery and heightened discomfort associated with delayed fracture healing present substantial clinical challenges. Investigations into lncRNA-mediated pathways may provide novel biological targets for enhancing osseous regeneration and improving clinical outcomes.</p><p><strong>Aim: </strong>The focus of this study is to elucidate the role and molecular mechanism of lncRNA LINC01123 (LINC01123) dysregulation in the osteogenic differentiation of osteoblasts.</p><p><strong>Methods: </strong>Real-time quantitative polymerase chain reaction (RT-qPCR) determined LINC01123, miR-134-5p and XIAP levels in samples, alongside an assessment of osteogenic marker mRNA expression. The targeting relationships were verified by luciferase activity assay. The biological behavioural competence of the cells was assessed by cell counting kit-8 (CCK-8), flow cytometry, alizarin red staining assay, and western blot assay. Receiver operating characteristic (ROC) curve was applied to analyse the potential of LINC01123 in the diagnosis of delayed fracture healing.</p><p><strong>Results: </strong>LINC01123 was overexpressed in patients experiencing delayed fractures and was sensitive in predicting the occurrence of delayed healing. As osteoblast differentiation progressed, the expression of LINC01123 and XIAP diminished, while the levels of miR-134-5p and ALP, OCN, RUNX2 mRNA were notably upregulated. Upregulation of LINC01123 reduced the levels of osteogenic biomarkers while suppressing cell viability and accelerating apoptosis, while miR-134-5p mimic partially reversed the inhibitory effect of LINC01123. Knockdown of XIAP partially mitigated the negative impact of silencing miR-134-5p on osteoblast differentiation and proliferation.</p><p><strong>Conclusion: </strong>Elevated LINC01123 expression promotes delayed fracture healing through the miR-134-5p/XIAP pathway, positioning it as a candidate prognostic marker for progression of fracture healing response.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":16629,"journal":{"name":"Journal of Orthopaedic Surgery and Research","volume":"20 1","pages":"790"},"PeriodicalIF":2.8000,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374377/pdf/","citationCount":"0","resultStr":"{\"title\":\"LncRNA LINC01123-mediated impaired fracture healing through miR-134-5p/XIAP axis.\",\"authors\":\"Song Zhou, ZeWen Zheng, ChuanKai Zhang, Liang Hao, Qiang Chen, Ke Sun, Min Cai\",\"doi\":\"10.1186/s13018-025-06167-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The prolonged recovery and heightened discomfort associated with delayed fracture healing present substantial clinical challenges. Investigations into lncRNA-mediated pathways may provide novel biological targets for enhancing osseous regeneration and improving clinical outcomes.</p><p><strong>Aim: </strong>The focus of this study is to elucidate the role and molecular mechanism of lncRNA LINC01123 (LINC01123) dysregulation in the osteogenic differentiation of osteoblasts.</p><p><strong>Methods: </strong>Real-time quantitative polymerase chain reaction (RT-qPCR) determined LINC01123, miR-134-5p and XIAP levels in samples, alongside an assessment of osteogenic marker mRNA expression. The targeting relationships were verified by luciferase activity assay. The biological behavioural competence of the cells was assessed by cell counting kit-8 (CCK-8), flow cytometry, alizarin red staining assay, and western blot assay. Receiver operating characteristic (ROC) curve was applied to analyse the potential of LINC01123 in the diagnosis of delayed fracture healing.</p><p><strong>Results: </strong>LINC01123 was overexpressed in patients experiencing delayed fractures and was sensitive in predicting the occurrence of delayed healing. As osteoblast differentiation progressed, the expression of LINC01123 and XIAP diminished, while the levels of miR-134-5p and ALP, OCN, RUNX2 mRNA were notably upregulated. Upregulation of LINC01123 reduced the levels of osteogenic biomarkers while suppressing cell viability and accelerating apoptosis, while miR-134-5p mimic partially reversed the inhibitory effect of LINC01123. Knockdown of XIAP partially mitigated the negative impact of silencing miR-134-5p on osteoblast differentiation and proliferation.</p><p><strong>Conclusion: </strong>Elevated LINC01123 expression promotes delayed fracture healing through the miR-134-5p/XIAP pathway, positioning it as a candidate prognostic marker for progression of fracture healing response.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>\",\"PeriodicalId\":16629,\"journal\":{\"name\":\"Journal of Orthopaedic Surgery and Research\",\"volume\":\"20 1\",\"pages\":\"790\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-08-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374377/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Orthopaedic Surgery and Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13018-025-06167-3\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ORTHOPEDICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Orthopaedic Surgery and Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13018-025-06167-3","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ORTHOPEDICS","Score":null,"Total":0}
LncRNA LINC01123-mediated impaired fracture healing through miR-134-5p/XIAP axis.
Background: The prolonged recovery and heightened discomfort associated with delayed fracture healing present substantial clinical challenges. Investigations into lncRNA-mediated pathways may provide novel biological targets for enhancing osseous regeneration and improving clinical outcomes.
Aim: The focus of this study is to elucidate the role and molecular mechanism of lncRNA LINC01123 (LINC01123) dysregulation in the osteogenic differentiation of osteoblasts.
Methods: Real-time quantitative polymerase chain reaction (RT-qPCR) determined LINC01123, miR-134-5p and XIAP levels in samples, alongside an assessment of osteogenic marker mRNA expression. The targeting relationships were verified by luciferase activity assay. The biological behavioural competence of the cells was assessed by cell counting kit-8 (CCK-8), flow cytometry, alizarin red staining assay, and western blot assay. Receiver operating characteristic (ROC) curve was applied to analyse the potential of LINC01123 in the diagnosis of delayed fracture healing.
Results: LINC01123 was overexpressed in patients experiencing delayed fractures and was sensitive in predicting the occurrence of delayed healing. As osteoblast differentiation progressed, the expression of LINC01123 and XIAP diminished, while the levels of miR-134-5p and ALP, OCN, RUNX2 mRNA were notably upregulated. Upregulation of LINC01123 reduced the levels of osteogenic biomarkers while suppressing cell viability and accelerating apoptosis, while miR-134-5p mimic partially reversed the inhibitory effect of LINC01123. Knockdown of XIAP partially mitigated the negative impact of silencing miR-134-5p on osteoblast differentiation and proliferation.
Conclusion: Elevated LINC01123 expression promotes delayed fracture healing through the miR-134-5p/XIAP pathway, positioning it as a candidate prognostic marker for progression of fracture healing response.
期刊介绍：
Journal of Orthopaedic Surgery and Research is an open access journal that encompasses all aspects of clinical and basic research studies related to musculoskeletal issues.
Orthopaedic research is conducted at clinical and basic science levels. With the advancement of new technologies and the increasing expectation and demand from doctors and patients, we are witnessing an enormous growth in clinical orthopaedic research, particularly in the fields of traumatology, spinal surgery, joint replacement, sports medicine, musculoskeletal tumour management, hand microsurgery, foot and ankle surgery, paediatric orthopaedic, and orthopaedic rehabilitation. The involvement of basic science ranges from molecular, cellular, structural and functional perspectives to tissue engineering, gait analysis, automation and robotic surgery. Implant and biomaterial designs are new disciplines that complement clinical applications.
JOSR encourages the publication of multidisciplinary research with collaboration amongst clinicians and scientists from different disciplines, which will be the trend in the coming decades.
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