Background and Purpose. Intervertebral disc degeneration (IDD) is the main cause of low back pain, but its pathogenesis has not been studied clearly. Circular RNA is a type of noncoding RNA (ncRNA). In this study, we studied the potential role of circular RNA in the pathogenesis of IDD. Methods. We obtained microarray data (GSE116726, GSE67566) from Gene Expression Omnibus database, and differential expression level of ncRNA in nucleus pulposus (NP) tissues of IDD patients was analyzed. The potential circRNA-miRNA-mRNA regulatory network was analyzed by starBase. The effect of the interaction between hsa_circ_0001658, hsa-miR-181c-5p, and FAS on the proliferation and apoptosis of human neural progenitor cells (hNPCs) was studied. Results. hsa_circ_0001658 was significantly upregulated ( logFC > 2.0 and adj . P . Val < 0.01 ) in the NP tissues of IDD patients, and hsa-miR-181c-5p expression was downregulated ( logFC < − 2.0 and adj . P . Val < 0.01 ). Silencing of hsa-miR-181c-5p or overexpression of hsa_circ_0001658 inhibited the proliferation of hNPCs and promoted their apoptosis. hsa_circ_0001658 acted as a sponge of hsa-miR-181c-5p. hsa-miR-181c-5p downregulated the expression of Fas cell surface death receptor (FAS), promoted the proliferation, and inhibited the apoptosis of hNPCs. hsa_circ_0001658 functioned in hNPCs through targeting hsa-miR-181c-5p/FAS. Conclusion. Circular RNA hsa_circ_0001658 inhibits IDD development by regulating hsa-miR-181c-5p/FAS. It is expected to be a potential target for the therapy of IDD.
Background and purpose: Intervertebral disc degeneration (IDD) is the main cause of low back pain, but its pathogenesis has not been studied clearly. Circular RNA is a type of non-coding RNA (ncRNA). In this study, we aim to study the potential role of circular RNA in the pathogenesis of IDD. Methods: We obtained microarray data (GSE116726, GSE67566) from Gene Expression Omnibus database, and differentially analyzed ncRNA in nucleus pulposus (NP) tissues of IDD patients. The potential circRNAs-miRNAs-mRNAs regulatory network was analyzed by starBase. The effect of the interaction between hsa_circ_0001658, hsa-miR-181c-5p and FAS on the proliferation and apoptosis of human neural progenitor cells (hNPCs) were studied. Results:Hsa_circ_0001658 was significantly up-regulated (logFC>2.0 and adj.P.Val<0.01) in the NP tissues of IDD patients, and hsa-miR-181c-5p expression was down-regulated (logFC<-2.0 and adj.P.Val<0.01). Silencing of hsa-miR-181c-5p or overexpression of hsa_circ_0001658 inhibited the proliferation of hNPCs and promoted their apoptosis. Hsa_circ_0001658 acted as a sponge of hsa-miR-181c-5p. Hsa-miR-181c-5p down-regulated the expression of FAS, promoted the proliferation and inhibited the apoptosis of hNPCs. Hsa_circ_0001658 functioned in hNPCs through targeting hsa-miR-181c-5p/FAS.Conclusion:Circular RNA hsa_circ_0001658 inhibits intervertebral disc degeneration development by regulating hsa-miR-181c-5p/FAS. It is expected to be a potential target for the therapy of IDD.
Background: Human DNA methylation is a common epigenetic regulatory mechanism, and it plays a critical role in various diseases. However, the potential role of DNA methylation in Ewing sarcoma (ES) is not clear. This study aimed to explore the regulatory roles of DNA methylation in ES. Methods:The microarray data of gene expression and methylation were downloaded from the Gene Expression Omnibus (GEO) database, and analyzed via GEO2R. Venn analysis was then applied to identify aberrantly methylated-differentially expressed genes (DEGs). Subsequently, function and pathway enrichment analysis was conducted, a protein-protein interaction (PPI) network was constructed, and hub genes were determined. Besides, a connectivity map (CMap) analysis was performed to screen bioactive compounds for ES treatment.Results: A total of 135 hypomethylated high expression genes and 523 hypermethylated low expression genes were identified. The hypomethylated high expression genes were enriched in signal transduction and the apoptosis process. Meanwhile, hypermethylated low expression genes were related to DNA replication and transcription regulation. The PPI network analysis indicated C3, TF, and TCEB1 might serve as diagnostic and therapeutic targets of ES. Furthermore, CMap analysis revealed 6 chemicals as potential options for ES treatment. Conclusions:The introduction of DNA methylation characteristics over DEGs is helpful to understand the pathogenesis of ES. The identified hub aberrantly methylated DEGs and chemicals might provide some novel insights on ES treatment.
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