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椎间盘退变的枢纽基因和关键途径：生物信息学分析和验证。

Hub Genes and Key Pathways of Intervertebral Disc Degeneration: Bioinformatics Analysis and Validation.

机构信息

College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan 430061, China.

Hubei Provincial Hospital of Traditional Chinese Medicine, No. 4, Garden Hill, Wuchang, Wuhan, Hubei 430061, China.

出版信息

Biomed Res Int. 2021 Sep 10;2021:5340449. doi: 10.1155/2021/5340449. eCollection 2021.

DOI:10.1155/2021/5340449
PMID:34545328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8449732/
Abstract

OBJECTIVE

To identify significant pathways and genes in intervertebral disc degeneration (IDD) based on bioinformatics analysis.

DESIGN

The GEO database was used to download the GSE124272 dataset. Differentially expressed genes (DEGs) were analyzed using Limma package in R language. Then, gene ontologies (GO), Kyoto encyclopedia of genes and genomes (KEGG), and protein-protein interaction (PPI) networks were used to further identify hub genes. The mRNA expression levels of top six hub genes were verified.

RESULTS

We found 563 DEGs, of which 214 were upregulated and 349 were downregulated. The top 5 GO terms and pathways were shown including immune response, cell cycle, and p53 pathway. Based on the PPI analysis, we verified the mRNA expression levels of 6 hub genes. The mRNA levels of CHEK1, CDCA2, SKA3, and KIF20A were upregulated in degenerative NP tissue than in healthy NP tissue. However, the mRNA level of BUB1 and SPC25 was downregulated.

CONCLUSIONS

This study may provide new biomarkers for the IDD and treatments to repair IDD related to CHEK1, CDCA2, SKA3, BUB1, KIF20A, and SPC25.

摘要

目的

基于生物信息学分析鉴定椎间盘退变（IDD）中的显著通路和基因。

设计

从 GEO 数据库中下载 GSE124272 数据集。使用 R 语言中的 Limma 软件包分析差异表达基因（DEGs）。然后，使用基因本体论（GO）、京都基因与基因组百科全书（KEGG）和蛋白质-蛋白质相互作用（PPI）网络进一步鉴定枢纽基因。验证前 6 个枢纽基因的 mRNA 表达水平。

结果

我们发现了 563 个 DEGs，其中 214 个上调，349 个下调。前 5 个 GO 术语和通路包括免疫反应、细胞周期和 p53 通路。基于 PPI 分析，我们验证了 6 个枢纽基因的 mRNA 表达水平。在退变的 NP 组织中，CHEK1、CDCA2、SKA3 和 KIF20A 的 mRNA 水平上调，而 BUB1 和 SPC25 的 mRNA 水平下调。

结论

本研究可能为 IDD 提供新的生物标志物，并为修复与 CHEK1、CDCA2、SKA3、BUB1、KIF20A 和 SPC25 相关的 IDD 提供新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/dec90780c7d6/BMRI2021-5340449.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/db7cab1de3b1/BMRI2021-5340449.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/b02a7b914330/BMRI2021-5340449.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/d7752772be0b/BMRI2021-5340449.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/e6ec9827c92c/BMRI2021-5340449.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/1c4699016ccb/BMRI2021-5340449.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/dec90780c7d6/BMRI2021-5340449.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/db7cab1de3b1/BMRI2021-5340449.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/b02a7b914330/BMRI2021-5340449.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/d7752772be0b/BMRI2021-5340449.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/e6ec9827c92c/BMRI2021-5340449.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/1c4699016ccb/BMRI2021-5340449.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/8449732/dec90780c7d6/BMRI2021-5340449.006.jpg

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