1. Academic Validation
  2. LncRNA MIR100HG induces degenerative changes in intervertebral disc degeneration nucleus pulposus cells by targeting miR-31-5p

LncRNA MIR100HG induces degenerative changes in intervertebral disc degeneration nucleus pulposus cells by targeting miR-31-5p

  • J Orthop Surg Res. 2025 Nov 17;20(1):1003. doi: 10.1186/s13018-025-06379-7.
Jincai Tian # 1 Zhixin Li # 2 Feng Wang 3 Jiayue Zhang 4 Liqi Zhao 4 Yuhui Ji 3 Yingxuan Huang 5 6
Affiliations

Affiliations

  • 1 Spine Department, Yinchuan Guolong Orthopedic Hospital, Yinchuan, 750000, China.
  • 2 The First School of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, 750000, China.
  • 3 Department of Orthopedics, The Fourth People's Hospital of Shenzhen, Shenzhen, 518118, China.
  • 4 Department of Neurology, The Fourth People's Hospital of Shenzhen, Shenzhen, 518118, China.
  • 5 Guangxi Key Laboratory for Preclinical and Translational Research on Bone and Joint Degenerative Diseases, Baise, 533000, China. [email protected].
  • 6 Pediatric Intensive Care Unit, The Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18, Zhongshan 2nd Road, Youjiang District, Baise, 533000, China. [email protected].
  • # Contributed equally.
Abstract

Background: To investigate the regulatory role of LncRNA MIR100HG on the functional and inflammatory levels of nucleus pulposus cells (NPCs) in intervertebral disc degeneration (IDD).

Methods: A total of 183 patients (including 101 IDD patients) were included. Magnetic resonance imaging (MRI) assessed the degree of IDD. Intraoperative nucleus pulposus tissue was stored at - 80 °C. Logistic regression analysis identified risk factors for IDD. ROC analysis assessed the diagnostic value of LncRNA MIR100HG in predicting IDD. RT-qPCR detected gene expression, while CCK8 and flow cytometry observed cell proliferation and Apoptosis. ELISA detected inflammatory factor expression. DLR and RIP validated the target relationship of genes.

Results: LncRNA MIR100HG is upregulated in NP tissue from IDD patients and increases with rising Pfirrman grades. LncRNA MIR100HG is a risk factor for IDD patients and has diagnostic value in predicting IDD progression. Overexpression of LncRNA MIR100HG leads to slowed NPCs proliferation and extracellular matrix (ECM) synthesis, promoting Apoptosis, increased inflammation levels, and ECM degradation. miR-31-5p is downregulated in NP tissue from IDD patients. LncRNA MIR100HG regulates NPCs function via miR-31-5p. Transfection of miR mimic can counteract the functional alterations in NPCs caused by LncRNA MIR100HG overexpression.

Conclusions: LncRNA MIR100HG targets miR-31-5p to inhibit NPCs proliferation and ECM anabolic metabolite expression, promote NPCs Apoptosis and increased inflammatory levels, thereby inducing degenerative changes in NPCs.

Keywords

LncRNA MIR100HG; miR-31-5p; Degeneration; Intervertebral disc; Nucleus pulposus.

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