Long Noncoding RNA SLC20A1-1 Induces Nucleus Pulposus Apoptosis by Sponging miR-146a-5p

Abstract

Background: Intervertebral disc degeneration (IDD) is a common cause of lower back pain and is characterized by cellular apoptosis, senescence, and extracellular matrix degradation. In the current study, we aimed to identify the effect of the long noncoding RNA SLC20A1-1 on tumor necrosis factor α (TNF-α)-induced apoptosis of nuclear pulposus cells (NPCs). Materials and Methods: NPCs were induced by TNF-α and used as an in vitro model. The mRNA expression of SLC20A1-1 was detected by quantitative real-time PCR (qPCR) both in clinical samples and in vitro. The scratch assay, Transwell invasion assay, CCK-8 assay, and flow cytometry were used to measure cell migration, growth, and apoptosis. The binding site between SLC20A1-1 and miR-146a-5p was assessed by a dual-luciferase reporter assay. Results: The expression of SLC20A1-1 was significantly upregulated in herniated lumbar discs, and TNF-α induced SLC20A1-1 expression in NPCs. Overexpression of SLC20A1-1 inhibited NPC growth, promoted NPC apoptosis, and enhanced macrophage recruitment and migration. The effect of SLC20A1-1 on NPCs and macrophages could be reversed by etanercept treatment. Moreover, we found that SLC20A1-1 could suppress miR-146a-5p to induce TRAF6 and caspase 3 expression. Conclusion: Overall, SLC20A1-1, an IDD regulator, is involved in TNF-α-induced NPC apoptosis by sponging miR-146a-5p. Clinical Trial Registration number: NMU20210325.