MicroRNA-25 protects nucleus pulposus cells against apoptosis via targeting SUMO2 in intervertebral disc degeneration
It has been reported that microRNA (miRNA/miR)-25 is downregulated in patients with intervertebral disc degeneration (IVDD). However, the potential role of miR-25 in IVDD remains unclear. Therefore, the present study aimed to investigate the effects of miR-25 on human intervertebral disc nucleus pul...
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Veröffentlicht in: | Molecular medicine reports 2021-10, Vol.24 (4), Article 724 |
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Sprache: | eng |
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Zusammenfassung: | It has been reported that microRNA (miRNA/miR)-25 is downregulated in patients with intervertebral disc degeneration (IVDD). However, the potential role of miR-25 in IVDD remains unclear. Therefore, the present study aimed to investigate the effects of miR-25 on human intervertebral disc nucleus pulposus cells (NPCs). The expression levels of miR-25 and those of small ubiquitin-related modifier 2 (SUMO2) were determined in human nucleus pulposus (NP) tissues by reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses. Subsequently, the potential interaction between miR-25 and SUMO2 was validated via dual-luciferase reporter assay and RNA pull-down assay with biotinylated miRNA. The effects of miR-25 on NPC proliferation and apoptosis were evaluated using Cell Counting Kit-8 assay, 5-ethynyl-2 '-deoxyuridine incorporation assay, and flow cytometry. The results showed that miR-25 was downregulated in patients with IVDD. In addition, miR-25 increased the proliferation of NPCs and inhibited their apoptosis. Furthermore, the current study verified that miR-25 could directly target SUMO2 and regulate its expression via the p53 signaling pathway. Additionally, the effects of miR-25 on NPCs were abrogated following SUMO2 overexpression. Overall, the results of the present study demonstrated that miR-25 could promote the proliferation and inhibit the apoptosis of NPCs via targeting SUMO2, suggesting that miR-25 may be a potential target in the treatment of IVDD. |
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ISSN: | 1791-2997 1791-3004 |
DOI: | 10.3892/mmr.2021.12363 |