The Prognostic Significance of LINC00638 in Lumbar Disc Herniation and Its Effect on Senescence of Nucleus Pulposus Cells

JOR Spine · Published 2025-12-01 · DOI 10.1002/jsp2.70138

Free full text

Authors being retrieved — see the publisher record. https://doi.org/10.1002/jsp2.70138

Abstract

ABSTRACT Background Lumbar disc herniation (LDH) is a common degenerative spinal disorder that severely impacts patients' quality of life. This study investigated the prognostic values of the lncRNA LINC00638 in LDH and its regulatory role in the senescence of human nucleus pulposus cells (hNPCs). Methods Serum was collected from 93 LDH patients and 108 healthy individuals (matched age and gender). RT‐qPCR was used to detect LINC00638 and miR‐185‐5p expression. The diagnostic and prognostic significance was analyzed using ROC and logistic regression. The hNPCs senescence model induced by 50 ng/mL TNF‐α was established to explore the effects of LINC00638 overexpression (alone or combined with miR‐185‐5p) on cell proliferation, apoptosis, senescence, inflammation, and oxidative stress. Results Serum LINC00638 levels in LDH patients gradually decreased with disease progression (p < 0.05) and were significantly correlated with VAS, JOA and ODI scores (p < 0.001). Low LINC00638 expression was identified as a reliable diagnostic indicator for LDH (AUC = 0.828, sensitivity 70.97%, specificity 80.56%, p < 0.001) and an independent risk factor for poor prognosis (OR = 0.176, p = 0.009). Cellular experiments showed that LINC00638 overexpression significantly inhibited TNF‐α‐induced cell senescence (p < 0.01), while this inhibitory effect was reversed by miR‐185‐5p overexpression (p < 0.05). Conclusions Serum LINC00638 holds promise as a potential biomarker for the diagnosis and prognostic evaluation of LDH, closely reflecting disease severity. Furthermore, LINC00638 participates in regulating hNPCs' senescence and LDH progression by modulating miR‐185‐5p.

Abstract from DOAJ. Public domain (CC0 1.0).

Read the article at the publisher →

Publication details

Year
2025

Related articles