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LINC00312 afecta la progresión de la osteoartritis al dirigirse al eje miR-331-3p/DUSP5

Dengke Zhao¹, Yiming Zhao¹, Yuxiang He¹

¹Department of Orthopedics, Qilu Hospital of Shandong University, 107 Wenhua West Road, Jinan, Shandong, 250012, China.

Journal of orthopaedic surgery and research

|February 14, 2026

Abstracto

Background:

As a chronic degenerative disease, osteoarthritis (OA) manifests through articular cartilage breakdown and ongoing inflammatory processes in joints. Recently, long non-coding RNAs (lncRNAs) have been participated in pathological process of OA through epigenetic regulation and molecular signaling axis.

Aim:

This study aimed to verify whether LINC00312 regulates DUSP5 expression by adsorbing miR-331-3p as a competitive endogenous RNA (ceRNA) in OA, thereby exerting a cartilage-protective effect.

Methods:

Expressions of LINC00312, miR-331-3p, and dual-specific protein phosphatase 5 (DUSP5) in patient tissues and chondrocytes were detected by reverse transcription-quantitative PCR (RT-qPCR). An in vitro OA model was constructed by stimulating chondrocytes with IL-1β. Cell viability and apoptosis were assessed via cell counting kit-8 (CCK-8) assays and flow cytometry. The levels of chondrogenic-related genes and proinflammatory factors were detected by RT-qPCR and enzyme-linked immunosorbent assay (ELISA). Interaction of miR-331-3p with LINC00312 and DUSP5 was detected via dual luciferase assays and RIP assays. Correlation between LINC00312, miR-331-3p, and DUSP5 in patients with OA was analyzed using Pearson correlation analysis.

Results:

In OA patients' cartilage tissue and IL-1β-induced OA models, LINC00312 and DUSP5 expression decreased while miR-331- 3p expression increased. Overexpression of LINC00312 ameliorated cell injury induced by IL-1β stimulation, enhanced cell viability, and reduced apoptosis, MMP13, ADAMTS5, IL-6, and IL-8 levels. miR-331-3p negatively correlated with LINC00312, and upregulation of miR-331-3p reversed the protective effect of LINC00312. Additionally, DUSP5 was a direct target of miR-331-3p, and LINC00312 and miR-331-3p jointly regulated DUSP5 expression.

Conclusions:

LINC00312 alleviates IL-1β-induced chondrocyte inflammation and apoptosis by acting as a ceRNA to regulate the miR-331-3p/DUSP5 axis. This suggests that LINC00312 may serve as a novel therapeutic target for OA.

Palabras clave:

Condrocitos DUSP5 LINC00312 Osteoartritis miR-331-3p

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