[1]陈 科,陈继军,陈赵乐,等.CPT1C的表达水平与甲基化的关联及其对胃癌预后的影响[J].医学信息,2022,35(18):19-24.[doi:10.3969/j.issn.1006-1959.2022.18.005]
 CHEN Ke,CHEN Ji-jun,CHEN Zhao-le,et al.Correlation Between CPT1C Expression and Methylation and its Effect on Prognosis of Gastric Cancer[J].Journal of Medical Information,2022,35(18):19-24.[doi:10.3969/j.issn.1006-1959.2022.18.005]
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CPT1C的表达水平与甲基化的关联及其对胃癌预后的影响()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
35卷
期数:
2022年18期
页码:
19-24
栏目:
论著
出版日期:
2022-09-15

文章信息/Info

Title:
Correlation Between CPT1C Expression and Methylation and its Effect on Prognosis of Gastric Cancer
文章编号:
1006-1959(2022)18-0019-06
作者:
陈 科陈继军陈赵乐
(解放军空军军医大学第一附属医院急诊科,陕西 西安 710032)
Author(s):
CHEN KeCHEN Ji-junCHEN Zhao-leet al.
(Department of Emergency,the First Affiliated Hospital of PLA Air Force Military Medical University,Xi’an 710032,Shaanxi,China)
关键词:
胃癌肿瘤基因组图谱Kaplan-Meier PlotterDNA甲基化交互可视化数据库CPT1C
Keywords:
Gastric cancerThe Cancer Genome AtlasKaplan-Meier PlotterDNA methylation interactive visualization databaseCPT1C
分类号:
R735.2
DOI:
10.3969/j.issn.1006-1959.2022.18.005
文献标志码:
A
摘要:
目的 探讨CPT1C在胃癌中的表达情况及其可能参与的信号通路。方法 从肿瘤基因组图谱(TCGA)数据库中下载并预处理胃癌数据集的mRNA表达RNA-seq数据及临床预后相关数据,对胃癌组织和正常组织中CPT1C基因进行差异表达分析,并绘制图型。以CPT1C表达量的中位数为界将胃癌患者分为高表达组和低表达组,使用Kaplan-Meier法进行生存分析,探索CPT1C的表达与胃癌患者生存和临床病理特征的关系。同时利用DNA甲基化交互可视化数据库(DNMIVD)分析CPT1C甲基化与基因表达的关系及其与预后的相关性。使用GSEA4.0.1软件进行基因集富集分析,同时进行多GSEA富集分析的图形绘制。结果 CPT1C在胃癌中显著高表达,与癌旁组织的差异具有统计学意义(P=0.003);删除TCGA胃癌患者中生存时间<30 d的样本后,共有306例样本,CPT1C高表达患者(n=153)预后更差(P=0.01),且在Kaplan-Meier Plotter数据分析平台中,高表达CPT1C的胃癌患者同样与不良预后相关(P<0.05);对TCGA胃癌患者的单因素和多因素回归分析提示,高表达CPT1C与更短的生存相关(P=0.02),CPT1C基因表达与DNA启动子甲基化呈显著负相关(r=-0.33,P=6.60e-10),并且低甲基化与不良预后相关(P=7.53e-03);GSEA分析结果显示,CPT1C高表达样本富集了ECM受体相互作用、Ca离子信号通路和HEDGEHOG信号通路等相关基因集,而CPT1C低表达样本则富集了剪接体,碱基切除修复和氧化磷酸化等相关基因集。结论 CPT1C可能作为胃癌的独立预后因素,其可能通过参与ECM受体相互作用、Ca离子信号通路和HEDGEHOG信号通路等通路调节胃癌的发生发展。
Abstract:
Objective To investigate the expression of CPT1C in gastric cancer and its possible signaling pathway.Methods The mRNA expression RNA-seq data and clinical prognosis related data of gastric cancer data set were downloaded and preprocessed from the Tumor Genome Atlas (TCGA) database to analyze the differential expression of CPT1C gene in gastric cancer tissues and normal tissues and draw the pattern. The gastric cancer patients were divided into high expression group and low expression group according to the median of CPT1C expression. Kaplan-Meier method was used for survival analysis to explore the relationship between CPT1C expression and survival and clinicopathological features of gastric cancer patients. The relationship between CPT1C methylation and gene expression and its correlation with prognosis were analyzed by DNA methylation interactive visual database (DNMIVD). GSEA 4.0.1 software was used for gene set enrichment analysis, and the graphics of multi-GSEA enrichment analysis were drawn.Results The expression of CPT1C was significantly higher in gastric cancer than that in adjacent tissues (P=0.003). After deleting the samples with survival time <30 days in TCGA gastric cancer patients, a total of 306 samples were obtained. Patients with high CPT1C expression (n=153) had a worse prognosis (P=0.01), and in the Kaplan-Meier Plotter data analysis platform, gastric cancer patients with high CPT1C expression were also associated with poor prognosis (P<0.05). Univariate and multivariate regression analysis of TCGA gastric cancer patients suggested that high expression of CPT1C was associated with shorter survival (P=0.02), CPT1C gene expression was significantly negatively correlated with DNA promoter methylation (r=-0.33, P=6.60e-10), and hypomethylation was associated with poor prognosis (P=7.53e-03). GSEA analysis showed that CPT1C high expression samples enriched ECM receptor interaction, Ca ion signaling pathway and HEDGEHOG signaling pathway related gene sets, while CPT1C low expression samples enriched spliceosome, base excision repair and oxidative phosphorylation related gene sets.Conclusion CPT1C may be an independent prognostic factor for gastric cancer, and it may regulate the occurrence and development of gastric cancer by participating in ECM receptor interaction, Ca ion signaling pathway and HEDGEHOG signaling pathway.

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更新日期/Last Update: 1900-01-01