文章摘要
朱芳丽,马晓莹,乔红,等.基于 GEO数据库对急性胰腺炎差异表达基因的分析及验证[J].安徽医药,2025,29(8):1618-1622.
基于 GEO数据库对急性胰腺炎差异表达基因的分析及验证
Analysis and verification of differentially expressed genes in acute pancreatitis based on GEO database
  
DOI:10.3969/j.issn.1009-6469.2025.08.026
中文关键词: 急性胰腺炎  差异基因表达  基因表达综合数据库  细胞周期素 D1  Smad蛋白质类  人微小核糖核酸
英文关键词: Acute pancreatitis  Differential gene expression  GEO database  Cyclin D1  Smad proteins  Human microRNA
基金项目:河北省秦皇岛科学技术研究与发展计划项目( 202101A080)
作者单位E-mail
朱芳丽 秦皇岛市第一医院消化内科,河北秦皇岛 066000  
马晓莹 秦皇岛市第一医院消化内科,河北秦皇岛 066000  
乔红 秦皇岛市第一医院消化内科,河北秦皇岛 066000  
刘烨 秦皇岛市第一医院消化内科,河北秦皇岛 066000  
杨悦 秦皇岛市第一医院消化内科,河北秦皇岛 066000  
韩俊岭 秦皇岛市第一医院消化内科,河北秦皇岛 066000 hanjunl00@163.com 
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中文摘要:
      目的基于基因表达综合数据库(GEO)分析急性胰腺炎( AP)病人基因表达差异,并进行验证。方法 2023年 9—12月从 GEO数据库下载基因表达综合系列(GSE)24279基因数据,使用 Bioconductor中的 Limma包筛选差异表达基因( DEGs);使用 Metascape及 String在线工具对差异表达基因进行功能富集分析,并使用 Cytoscape软件构建 AP相关基因及其靶标微小核糖核酸(miRNA)的调控网络图,最后使用反转录 -聚合酶链式扩增技术( RT-PCR)进行进一步验证。结果从 GEO数据库中共获取 53个 DEGs,其中 14个上调和 39个下调;并确定了 290个 DEGs的靶基因,在靶基因中 279个基因是 AP相关基因,同时又被调控网络中的 37个 miRNA靶向。其中人微小核糖核酸( hsa-miR)-15a、hsa-miR-16、hsa-miR-155、hsa-miR-375和 hsa-miR-429可能通过靶向调控网络中的基因参与 AP的发生发展过程中,且 hsa-miR-15a、hsa-miR-16及 hsa-miR-429靶向细胞周期素 D1(CCND1),hsa-miR-155靶向 CCND1和 Smad同源物 2(SMAD2),hsa-miR-375靶向丝氨酸 /苏氨酸激酶 2(AKT2)和周期素依赖性激酶 6(CDK6); RT-PCR结果显示, AP病人 hsa-miR-15a、hsa-miR-16基因表达水平( 1.49±0.35、1.01±0.20)高于健康体检者(1.12±0.24、0.80±0.26)(P<0.05)hsa-miR-429基因表达水平 0.90±0.23低于健康体检者 1.20±0.32(P<0.05)。结论 AP中 DEGs与疾病的发生进展相关,富集分析,和关键基因筛选为更深入研究 AP的发病机制和治疗靶点提供方向。
英文摘要:
      Objective To analyze and verify the differences of gene expression in patients with acute pancreatitis (AP) based on thecomprehensive gene expression omnibus (GEO).Methods From September 2023 to December 2023, the comprehensive Gene Expres-sion Omnibus(GSE) 24279 were downloaded from GEO database, and the differentially expressed genes (DEGs) were screened by Lim-ma package in Bioconductor. Metascape and String online tools were used to analyze the function enrichment of differentially expressedgenes, and Cytoscape software was used to construct the regulatory network diagram of AP-related genes and their target microRNAs (miRNA). Finally, reverse transcription-polymerase chain reaction (RT-PCR) was used for further verification.Results A total of 53DEGs were obtained from GEO database, of which 14 were up-regulated and 39 were down-regulated. 290 DEGs target genes were identified, among which 279 genes were AP-related genes, and at the same time they were targeted by 37 miRNA in the regulatory net-work. Among them, human micro ribonucleic acid (hsa-miR)-15a, hsa-miR-16, hsa-miR-155, hsa-miR-375 and hsa-miR-429 might be participated in the occurrence and development of AP through targeted regulation of genes in the network. Hsa-miR-15a, hsa-miR-16 and hsa-miR-429 targets cyclin D1 (CCND1), hsa-miR-155 targets CCND1 and Smad homologue 2 (SMAD2), and hsa-miR-375 targets serine/threonine kinase 2 (AKT2) and cyclin-dependent kinase 6 (CDK6). The RT-PCR results showed that the gene expression levels of hsa-miR-15a and hsa-miR-16 in AP patients (1.49 ± 0.35, 1.01 ± 0.20) were higher than those in healthy individuals (1.12 ± 0.24, 0.80 ± 0.26) (P<0.05). The gene expression level of hsa-miR-429 (0.90±0.23) was lower than that of healthy people (1.20±0.32) (P<0.05).Conclusions DEGs in AP is related to the occurrence and progress of the disease. Enrichment analysis and screening of key genes provide a direction for further study of the pathogenesis and therapeutic targets of AP.
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