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Background <p>This study was designed to investigate the diagnostic potential of the long non-coding RNA JPX in osteoporotic fractures (OPF) and to explore its functional role in the regulation of fracture healing.</p> Methods <p>A total of 244 patients with osteoporosis were enrolled, including 110 with osteoporosis (OP) and 134 with OPF. Expression levels of JPX, miR-219a-5p, and osteogenic markers (OPG, ALP, Collagen I, OCN) were detected by RT-qPCR. ROC analysis was employed to assess the clinical value of JPX. In human bone marrow mesenchymal stem cells (hBMSCs), gain- and loss-of-function experiments were performed to modulate JPX and miR-219a-5p expression. Cell proliferation was evaluated by CCK-8 assay. Flow cytometry assessed apoptosis. Dual luciferase reporter assays and RIP experiments validated the targeting relationship between JPX and miR-219a-5p.</p> Results <p>JPX was upregulated in the OPF group, with good diagnostic performance (AUC = 0.897; specificity = 76.87%; sensitivity = 84.55%), and JPX was identified an independent predictive factor. DFH and NFH could also be distinguished. JPX upregulation inhibited proliferation, promoted apoptosis, and suppressed osteogenic markers and ALP activity. JPX largely resides in the cytoplasm and directly binds miR-219a-5p, forming a ceRNA axis; upregulation of miR-219a-5p could reverse these effects.</p> Conclusion <p>JPX is associated with fracture risk and delayed healing, potentially influencing osteogenesis by sponge-like regulation of miR-219a-5p.</p>

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Diagnostic value of LncRNA JPX in osteoporotic fracture (OPF) and its role in inhibiting osteogenic differentiation by targeting miR-219a-5p

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月1日

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  • Junli Li,
  • Yiwei Li,
  • Ningning Zhang,
  • Zhijian Cheng

摘要

Background

This study was designed to investigate the diagnostic potential of the long non-coding RNA JPX in osteoporotic fractures (OPF) and to explore its functional role in the regulation of fracture healing.

Methods

A total of 244 patients with osteoporosis were enrolled, including 110 with osteoporosis (OP) and 134 with OPF. Expression levels of JPX, miR-219a-5p, and osteogenic markers (OPG, ALP, Collagen I, OCN) were detected by RT-qPCR. ROC analysis was employed to assess the clinical value of JPX. In human bone marrow mesenchymal stem cells (hBMSCs), gain- and loss-of-function experiments were performed to modulate JPX and miR-219a-5p expression. Cell proliferation was evaluated by CCK-8 assay. Flow cytometry assessed apoptosis. Dual luciferase reporter assays and RIP experiments validated the targeting relationship between JPX and miR-219a-5p.

Results

JPX was upregulated in the OPF group, with good diagnostic performance (AUC = 0.897; specificity = 76.87%; sensitivity = 84.55%), and JPX was identified an independent predictive factor. DFH and NFH could also be distinguished. JPX upregulation inhibited proliferation, promoted apoptosis, and suppressed osteogenic markers and ALP activity. JPX largely resides in the cytoplasm and directly binds miR-219a-5p, forming a ceRNA axis; upregulation of miR-219a-5p could reverse these effects.

Conclusion

JPX is associated with fracture risk and delayed healing, potentially influencing osteogenesis by sponge-like regulation of miR-219a-5p.