• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

鉴定并验证CDC20和ITCH作为特发性肺纤维化中泛素化相关生物标志物

Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis.

作者信息

Sun Shulei, Wang Yubao, Feng Jing

机构信息

Department of Respiratory and Critical Care Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.

出版信息

Hereditas. 2025 Apr 1;162(1):50. doi: 10.1186/s41065-025-00401-y.

DOI:10.1186/s41065-025-00401-y
PMID:40170095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11959808/
Abstract

PURPOSE

Ubiquitination plays a crucial role in various diseases. This study aims to explore the potential ubiquitination related genes in IPF.

METHODS

The gene microarray dataset GSE24206 was obtained from GEO database. Subsequently, through differential expression analysis and molecular signatures database, we obtained 1734 differentially expressed genes and 742 ubiquitination related genes. Through the venn diagram analysis, we obtained 53 differentially expressed ubiquitination related genes. Then, gene-ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, protein-protein interactions (PPI) and gene set enrichment analysis (GSEA) were applied for the differentially expressed ubiquitination related genes. Finally, the expression of CDC20 and ITCH in IPF patients and cells were validated by qPCR and western blot assay.

RESULTS

A total of 53 differentially expressed ubiquitination related genes (36 up-regulated genes and 17 down-regulated genes) were identified between 17 IPF patients and 6 healthy controls. GO and KEGG enrichment analysis of ubiquitination related genes mainly involved in regulation of protein ubiquitination, regulation of post-translational protein modification and ubiquitin mediated proteolysis. The PPI results demonstrated that these ubiquitination related genes interacted with each other. The GSEA analysis results for some of the hub genes mainly involved epithelial mesenchymal transition, inflammatory response, hypoxia, and apoptosis. The experiment expression level of CDC20 and ITCH in IPF patients and IPF cells were consistent with the bioinformatics analysis results.

CONCLUSION

We identified 53 potential ubiquitination related genes of IPF through bioinformatics analysis. CDC20 and ITCH and other ubiquitination related genes may influence the development of IPF through epithelial mesenchymal transition and inflammatory response. Our research findings provide insights into the mechanisms of fibrosis and may provide evidence for potential therapeutic targets for fibrosis.

摘要

目的

泛素化在多种疾病中起着关键作用。本研究旨在探索特发性肺纤维化（IPF）中潜在的泛素化相关基因。

方法

从基因表达综合数据库（GEO数据库）获取基因芯片数据集GSE24206。随后，通过差异表达分析和分子特征数据库，我们获得了1734个差异表达基因和742个泛素化相关基因。通过维恩图分析，我们获得了53个差异表达的泛素化相关基因。然后，对差异表达的泛素化相关基因进行基因本体（GO）富集分析、京都基因与基因组百科全书（KEGG）通路富集分析、蛋白质-蛋白质相互作用（PPI）和基因集富集分析（GSEA）。最后，通过定量聚合酶链反应（qPCR）和蛋白质免疫印迹法验证IPF患者和细胞中细胞分裂周期蛋白20（CDC20）和ITCH的表达。

结果

在17例IPF患者和6例健康对照之间共鉴定出53个差异表达的泛素化相关基因（36个上调基因和17个下调基因）。泛素化相关基因的GO和KEGG富集分析主要涉及蛋白质泛素化调节、翻译后蛋白质修饰调节和泛素介导的蛋白水解。PPI结果表明这些泛素化相关基因相互作用。一些枢纽基因的GSEA分析结果主要涉及上皮-间质转化、炎症反应、缺氧和细胞凋亡。IPF患者和IPF细胞中CDC20和ITCH的实验表达水平与生物信息学分析结果一致。

结论

我们通过生物信息学分析鉴定了53个IPF潜在的泛素化相关基因。CDC20和ITCH等泛素化相关基因可能通过上皮-间质转化和炎症反应影响IPF的发展。我们的研究结果为纤维化机制提供了见解，并可能为纤维化的潜在治疗靶点提供证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/b09a2bc334e8/41065_2025_401_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/651d00df99f5/41065_2025_401_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/c4e00b6e5c5f/41065_2025_401_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/ed232709ea0a/41065_2025_401_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/a0716fafe2b9/41065_2025_401_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/d64df3c4c94c/41065_2025_401_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/7361a708d3d5/41065_2025_401_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/d73df2dbeb55/41065_2025_401_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/526c61d5e52d/41065_2025_401_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/ba688073251f/41065_2025_401_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/5eeacc1ed053/41065_2025_401_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/a7bcf045f2fd/41065_2025_401_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/7fc33c76ea27/41065_2025_401_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/b09a2bc334e8/41065_2025_401_Fig13_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/651d00df99f5/41065_2025_401_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/c4e00b6e5c5f/41065_2025_401_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/ed232709ea0a/41065_2025_401_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/a0716fafe2b9/41065_2025_401_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/d64df3c4c94c/41065_2025_401_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/7361a708d3d5/41065_2025_401_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/d73df2dbeb55/41065_2025_401_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/526c61d5e52d/41065_2025_401_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/ba688073251f/41065_2025_401_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/5eeacc1ed053/41065_2025_401_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/a7bcf045f2fd/41065_2025_401_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/7fc33c76ea27/41065_2025_401_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a9b/11959808/b09a2bc334e8/41065_2025_401_Fig13_HTML.jpg

相似文献

1
Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis.鉴定并验证CDC20和ITCH作为特发性肺纤维化中泛素化相关生物标志物
Hereditas. 2025 Apr 1;162(1):50. doi: 10.1186/s41065-025-00401-y.
2
Identification of cell division cycle 20 as a candidate biomarker and potential therapeutic target in bladder cancer using bioinformatics analysis.使用生物信息学分析鉴定细胞周期蛋白 20 作为膀胱癌的候选生物标志物和潜在治疗靶点。
Biosci Rep. 2020 Jul 31;40(7). doi: 10.1042/BSR20194429.
3
Identification and Validation of Potential Biomarkers and Pathways for Idiopathic Pulmonary Fibrosis by Comprehensive Bioinformatics Analysis.综合生物信息学分析鉴定和验证特发性肺纤维化的潜在生物标志物和途径。
Biomed Res Int. 2021 Jul 4;2021:5545312. doi: 10.1155/2021/5545312. eCollection 2021.
4
Deciphering the Underlying Mechanisms of Sanleng-Ezhu for the Treatment of Idiopathic Pulmonary Fibrosis Based on Network Pharmacology and Single-cell RNA Sequencing Data.基于网络药理学和单细胞 RNA 测序数据解析三楞莪术治疗特发性肺纤维化的潜在机制。
Curr Comput Aided Drug Des. 2024;20(6):888-910. doi: 10.2174/1573409920666230808120504.
5
Transcriptomics in idiopathic pulmonary fibrosis unveiled: a new perspective from differentially expressed genes to therapeutic targets.特发性肺纤维化中的转录组学研究：从差异表达基因到治疗靶点的新视角。
Front Immunol. 2024 Mar 19;15:1375171. doi: 10.3389/fimmu.2024.1375171. eCollection 2024.
6
Identification of ubiquitination-related key biomarkers and immune infiltration in Crohn's disease by bioinformatics analysis and machine learning.通过生物信息学分析和机器学习鉴定克罗恩病中泛素化相关关键生物标志物及免疫浸润情况
Sci Rep. 2025 Jan 27;15(1):3444. doi: 10.1038/s41598-025-88148-4.
7
Identification and analysis of extracellular matrix and epithelial-mesenchymal transition-related genes in idiopathic pulmonary fibrosis by bioinformatics analysis and experimental validation.通过生物信息学分析和实验验证对特发性肺纤维化中细胞外基质和上皮-间质转化相关基因进行鉴定与分析
Gene. 2025 Jul 10;956:149464. doi: 10.1016/j.gene.2025.149464. Epub 2025 Apr 3.
8
Prediction model of mitochondrial energy metabolism related genes in idiopathic pulmonary fibrosis and its correlation with immune microenvironment.特发性肺纤维化中线粒体能量代谢相关基因的预测模型及其与免疫微环境的相关性
Sci Rep. 2025 May 14;15(1):16801. doi: 10.1038/s41598-025-01759-9.
9
Prediction and analysis of genetic effect in idiopathic pulmonary fibrosis and gastroesophageal reflux disease.特发性肺纤维化和胃食管反流病的遗传效应预测与分析。
IET Syst Biol. 2023 Dec;17(6):352-365. doi: 10.1049/syb2.12081. Epub 2023 Oct 31.
10
Underlying Molecular Mechanism and Construction of a miRNA-Gene Network in Idiopathic Pulmonary Fibrosis by Bioinformatics.生物信息学方法研究特发性肺纤维化中 miRNA-基因网络的潜在分子机制与构建
Int J Mol Sci. 2023 Aug 27;24(17):13305. doi: 10.3390/ijms241713305.

本文引用的文献

1
Bortezomib enhances the efficacy of BCMA CAR-T therapy through up-regulating BCMA expression in myeloma cells.硼替佐米通过上调骨髓瘤细胞中BCMA的表达来增强BCMA嵌合抗原受体T细胞（CAR-T）疗法的疗效。
Int Immunopharmacol. 2025 Feb 20;148:114113. doi: 10.1016/j.intimp.2025.114113. Epub 2025 Jan 24.
2
Hexamethylene amiloride induces lysosome-mediated cell death in multiple myeloma through transcription factor E3.六亚甲基阿米洛利通过转录因子E3诱导多发性骨髓瘤细胞发生溶酶体介导的细胞死亡。
Cell Death Discov. 2024 Dec 18;10(1):505. doi: 10.1038/s41420-024-02269-9.
3
Biological and pharmacological roles of pyroptosis in pulmonary inflammation and fibrosis: recent advances and future directions.
细胞焦亡在肺部炎症和纤维化中的生物学及药理学作用：最新进展与未来方向
Cell Commun Signal. 2024 Dec 5;22(1):586. doi: 10.1186/s12964-024-01966-3.
4
The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19.上皮-间充质转化在肺纤维化中的作用：特发性肺纤维化和 COVID-19 的启示。
Cell Commun Signal. 2024 Nov 13;22(1):542. doi: 10.1186/s12964-024-01925-y.
5
USP7 deubiquitinates KRAS and promotes non-small cell lung cancer.USP7 去泛素化 KRAS 并促进非小细胞肺癌。
Cell Rep. 2024 Nov 26;43(11):114917. doi: 10.1016/j.celrep.2024.114917. Epub 2024 Nov 4.
6
OAS3 Deubiquitination Due to E3 Ligase TRIM21 Downregulation Promotes Epithelial Cell Apoptosis and Drives Sepsis-induced Acute Lung Injury.OAS3 通过去泛素化酶 E3 连接酶 TRIM21 的下调促进上皮细胞凋亡并驱动脓毒症诱导的急性肺损伤。
Int J Biol Sci. 2024 Oct 14;20(14):5594-5607. doi: 10.7150/ijbs.96089. eCollection 2024.
7
MiR-125b-5p alleviates pulmonary fibrosis by inhibiting TGFβ1-mediated epithelial-mesenchymal transition via targeting BAK1.miR-125b-5p 通过靶向 BAK1 抑制 TGFβ1 介导的上皮-间充质转化缓解肺纤维化。
Respir Res. 2024 Oct 19;25(1):382. doi: 10.1186/s12931-024-03011-w.
8
Implications of ITCH-mediated ubiquitination of SIX1 on CDC27-cyclinB1 signaling in nasopharyngeal carcinoma.ITC 介导的 SIX1 泛素化对鼻咽癌中 CDC27-cyclinB1 信号的影响。
Sci Rep. 2024 Oct 15;14(1):24140. doi: 10.1038/s41598-024-73239-5.
9
The role of ubiquitination in health and disease.泛素化在健康与疾病中的作用。
MedComm (2020). 2024 Sep 25;5(10):e736. doi: 10.1002/mco2.736. eCollection 2024 Oct.
10
Deubiquitinase USP18 inhibits hepatic stellate cells activation and alleviates liver fibrosis via regulation of TAK1 activity.去泛素化酶 USP18 通过调节 TAK1 活性抑制肝星状细胞激活并减轻肝纤维化。
Exp Cell Res. 2024 Oct 1;442(2):114235. doi: 10.1016/j.yexcr.2024.114235. Epub 2024 Sep 3.