DOI: 10.1515/tjb-2025-0499 ISSN: 1303-829X

Analysis of RAMP2-AS1 as biomarkers of osteoarthritis and its clinical value

Menglei Hu, Haidong Zhou, Changtai Luo, Yibing Liu

Abstracts

Objectives

Osteoarthritis (OA) is a prevalent degenerative joint disorder. Non-coding RNAs (e.g., lncRNAs) have been increasingly implicated in OA progression, but their precise mechanisms remain to be elucidated. This study aimed to investigate the expression pattern and diagnostic value of lncRNA RAMP2-AS1 in OA and elucidate its regulatory role in chondrocyte function.

Methods

Differentially expressed lncRNAs in OA were identified through bioinformatics analysis of the GSE263210 dataset. RT-qPCR was used to measure the expression levels of RAMP2-AS1 and miR-328-3p in cartilage tissues from OA patients and healthy controls. The diagnostic efficacy of RAMP2-AS1 was evaluated using receiver operating characteristic (ROC) curve analysis. In vitro , IL-1β-treated C28/I2 cells were used to mimic OA conditions, and transfection techniques were employed to modulate RAMP2-AS1 and miR-328-3p expression. Cell proliferation was assessed using the CCK-8 assay, migration and invasion were examined using Transwell assays, and apoptosis was analyzed by flow cytometry. The targeting relationship between RAMP2-AS1 and miR-328-3p was validated by dual-luciferase reporter assay. Statistical analysis was performed using t-tests, ANOVA, and Spearman correlation.

Results

RAMP2-AS1 was significantly upregulated in OA patients and exhibited high diagnostic value (AUC=0.894). Its expression was negatively correlated with miR-328-3p and directly targeted miR-328-3p. Functional assays demonstrated that RAMP2-AS1 overexpression inhibited chondrocyte proliferation, migration, and invasion, while promoting apoptosis; these effects were reversed by miR-328-3p.

Conclusions

RAMP2-AS1 is highly expressed in OA and may serve as a diagnostic biomarker. It regulates chondrocyte function by targeting miR-328-3p, suggesting its potential as a therapeutic target for OA.

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