{"title":"肝细胞癌预后标志物的生物信息学筛选。","authors":"Chunxu Bao, Tingting Liu, Guiling Hu, Wentao Gao, Lin Sun, Xiaoping Ma, Jianshe Wei","doi":"10.1177/18758592241304994","DOIUrl":null,"url":null,"abstract":"<p><p>BackgroundThis study aimed to identify hub genes linked to hepatocellular carcinoma (LIHC) pathogenesis using bioinformatics analysis.MethodA total of 3865 samples from 12 datasets in the HCCDB database were analyzed to identify prognostic expression genes (PDGs). Enrichment analysis using DAVID and GSCA databases unveiled biological processes and signaling pathways associated with PDGs. Cytohubba app was utilized to identify 6 hub genes from the PDGs. Verification of hub genes was conducted using three GEO datasets and Western blot. Histopathological staining data of hub genes in LIHC patients were retrieved from the Human Protein Atlas database. Comprehensive analyses of hub genes were performed, including immune infiltration, prognosis, survival, methylation, gene mutation, related miRNA, and single-cell type. Potential therapeutic drugs were predicted using GDSC and CTRP databases.ResultA total of 1259 differential genes were screened, yielding 82 PDGs (36 up-regulated and 46 down-regulated genes). Hub genes identified included CDC20, TOP2A, CDK1 (up-regulated), and CAT, TAT, FTCD (down-regulated). These hub genes exhibited strong associations with immune cells and showed promising prognostic value based on AUC analysis. Reduced promoter methylation levels of TOP2A, CDK1, and FTCD in LIHC were observed. Single nucleotide polymorphisms analysis highlighted prevalent variants and miRNA expression associations impacting patient survival. Hub genes were enriched in various cell types. Trametinib, selumetinib, RDEA119, and teniposide were identified as potential drugs for LIHC treatment.ConclusionCDC20, TOP2A, CDK1, CAT, TAT, and FTCD may contribute to LIHC development and serve as novel prognostic biomarkers.</p>","PeriodicalId":56320,"journal":{"name":"Cancer Biomarkers","volume":"42 2","pages":"18758592241304994"},"PeriodicalIF":2.2000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bioinformatics screened of biomarkers for the prognosis of hepatocellular carcinoma.\",\"authors\":\"Chunxu Bao, Tingting Liu, Guiling Hu, Wentao Gao, Lin Sun, Xiaoping Ma, Jianshe Wei\",\"doi\":\"10.1177/18758592241304994\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>BackgroundThis study aimed to identify hub genes linked to hepatocellular carcinoma (LIHC) pathogenesis using bioinformatics analysis.MethodA total of 3865 samples from 12 datasets in the HCCDB database were analyzed to identify prognostic expression genes (PDGs). Enrichment analysis using DAVID and GSCA databases unveiled biological processes and signaling pathways associated with PDGs. Cytohubba app was utilized to identify 6 hub genes from the PDGs. Verification of hub genes was conducted using three GEO datasets and Western blot. Histopathological staining data of hub genes in LIHC patients were retrieved from the Human Protein Atlas database. Comprehensive analyses of hub genes were performed, including immune infiltration, prognosis, survival, methylation, gene mutation, related miRNA, and single-cell type. Potential therapeutic drugs were predicted using GDSC and CTRP databases.ResultA total of 1259 differential genes were screened, yielding 82 PDGs (36 up-regulated and 46 down-regulated genes). Hub genes identified included CDC20, TOP2A, CDK1 (up-regulated), and CAT, TAT, FTCD (down-regulated). These hub genes exhibited strong associations with immune cells and showed promising prognostic value based on AUC analysis. Reduced promoter methylation levels of TOP2A, CDK1, and FTCD in LIHC were observed. Single nucleotide polymorphisms analysis highlighted prevalent variants and miRNA expression associations impacting patient survival. Hub genes were enriched in various cell types. Trametinib, selumetinib, RDEA119, and teniposide were identified as potential drugs for LIHC treatment.ConclusionCDC20, TOP2A, CDK1, CAT, TAT, and FTCD may contribute to LIHC development and serve as novel prognostic biomarkers.</p>\",\"PeriodicalId\":56320,\"journal\":{\"name\":\"Cancer Biomarkers\",\"volume\":\"42 2\",\"pages\":\"18758592241304994\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Biomarkers\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1177/18758592241304994\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/3 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biomarkers","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/18758592241304994","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/3 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
背景:本研究旨在通过生物信息学分析确定与肝细胞癌(LIHC)发病机制相关的枢纽基因。方法分析HCCDB数据库中12个数据集的3865个样本,鉴定预后表达基因(PDGs)。利用DAVID和GSCA数据库进行富集分析,揭示了与PDGs相关的生物过程和信号通路。利用Cytohubba app从PDGs中鉴定出6个枢纽基因。利用三个GEO数据集和Western blot对枢纽基因进行验证。LIHC患者中心基因的组织病理学染色数据从Human Protein Atlas数据库中检索。对枢纽基因进行综合分析,包括免疫浸润、预后、生存、甲基化、基因突变、相关miRNA和单细胞类型。利用GDSC和CTRP数据库预测潜在的治疗药物。结果共筛选到1259个差异基因,得到82个PDGs,其中上调36个,下调46个。中心基因包括CDC20、TOP2A、CDK1(上调)和CAT、TAT、FTCD(下调)。这些枢纽基因显示出与免疫细胞的强相关性,并基于AUC分析显示出有希望的预后价值。观察到LIHC中TOP2A、CDK1和FTCD启动子甲基化水平降低。单核苷酸多态性分析强调了影响患者生存的流行变异和miRNA表达关联。Hub基因在多种细胞类型中均有富集。曲美替尼、塞鲁美替尼、RDEA119和替尼泊苷被确定为LIHC治疗的潜在药物。结论cdc20、TOP2A、CDK1、CAT、TAT和FTCD可能参与LIHC的发展,并可作为新的预后生物标志物。
Bioinformatics screened of biomarkers for the prognosis of hepatocellular carcinoma.
BackgroundThis study aimed to identify hub genes linked to hepatocellular carcinoma (LIHC) pathogenesis using bioinformatics analysis.MethodA total of 3865 samples from 12 datasets in the HCCDB database were analyzed to identify prognostic expression genes (PDGs). Enrichment analysis using DAVID and GSCA databases unveiled biological processes and signaling pathways associated with PDGs. Cytohubba app was utilized to identify 6 hub genes from the PDGs. Verification of hub genes was conducted using three GEO datasets and Western blot. Histopathological staining data of hub genes in LIHC patients were retrieved from the Human Protein Atlas database. Comprehensive analyses of hub genes were performed, including immune infiltration, prognosis, survival, methylation, gene mutation, related miRNA, and single-cell type. Potential therapeutic drugs were predicted using GDSC and CTRP databases.ResultA total of 1259 differential genes were screened, yielding 82 PDGs (36 up-regulated and 46 down-regulated genes). Hub genes identified included CDC20, TOP2A, CDK1 (up-regulated), and CAT, TAT, FTCD (down-regulated). These hub genes exhibited strong associations with immune cells and showed promising prognostic value based on AUC analysis. Reduced promoter methylation levels of TOP2A, CDK1, and FTCD in LIHC were observed. Single nucleotide polymorphisms analysis highlighted prevalent variants and miRNA expression associations impacting patient survival. Hub genes were enriched in various cell types. Trametinib, selumetinib, RDEA119, and teniposide were identified as potential drugs for LIHC treatment.ConclusionCDC20, TOP2A, CDK1, CAT, TAT, and FTCD may contribute to LIHC development and serve as novel prognostic biomarkers.
期刊介绍:
Concentrating on molecular biomarkers in cancer research, Cancer Biomarkers publishes original research findings (and reviews solicited by the editor) on the subject of the identification of markers associated with the disease processes whether or not they are an integral part of the pathological lesion.
The disease markers may include, but are not limited to, genomic, epigenomic, proteomics, cellular and morphologic, and genetic factors predisposing to the disease or indicating the occurrence of the disease. Manuscripts on these factors or biomarkers, either in altered forms, abnormal concentrations or with abnormal tissue distribution leading to disease causation will be accepted.