This study aimed to investigate the molecular mechanism by which microRNA (miR)-96 regulates the progression of intervertebral disc degeneration (IDD). The expression of miR-96 in normal intervertebral discs and in IDD was detected by performing reverse transcription-quantitative PCR. CCK8 assay was applied to examine the proliferation of nucleus pulpous (NP) cells and flow cytometry was used to evaluate the cell apoptosis and cell cycle profile. In addition, the immunofluorescence analysis was employed to detect cell proliferation. The expressions of proteins were assessed by western blot analysis. TargetScan and miRDB were used to predict the target genes of miR-96. The results indicated that miR-96 expression was upregulated in IDD compared with normal intervertebral discs. Overexpression of miR-96 could significantly inhibit the proliferation of NP cells via inducing apoptosis and G1 arrest. In addition, fibroblast growth factor receptor substrate 2 (FRS2) was identified as the target of miR-96 and overexpression of FRS2 could revere the effect of miR-96 mimics in NP cells. Therefore, these findings demonstrated that miR-96 plays a critical role during the progression of IDD and miR-96 may serve as a target for the treatment of IDD.

这项研究旨在调查的分子机制，microRNA（miR）-96调节椎间盘退变（IDD）的进程。通过进行逆转录定量PCR检测miR-96在正常椎间盘和IDD中的表达。采用CCK8法检测髓核（NP）细胞的增殖，采用流式细胞术评估细胞凋亡和细胞周期情况。另外，采用免疫荧光分析来检测细胞增殖。通过蛋白质印迹分析评估蛋白质的表达。使用TargetScan和miRDB预测miR-96的靶基因。结果表明与正常椎间盘相比，IDR中的miR-96表达上调。miR-96的过表达可通过诱导细胞凋亡和G1阻滞来显着抑制NP细胞的增殖。此外，成纤维细胞生长因子受体底物2（FRS2）被确定为miR-96的靶标，而FRS2的过表达可以证明miR-96模拟物在NP细胞中的作用。因此，这些发现表明，miR-96在IDD进程中起关键作用，而miR-96可能作为IDD治疗的靶标。