Expression of the Circadian Clock Gene ARNTL associated with DNA repair gene and prognosis of patient with osteosarcoma

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2022-07-01 DOI:10.1016/j.mrfmmm.2022.111801

Daliang Kong , Yang Liu , Minglei Zhang

{"title":"Expression of the Circadian Clock Gene ARNTL associated with DNA repair gene and prognosis of patient with osteosarcoma","authors":"Daliang Kong , Yang Liu , Minglei Zhang","doi":"10.1016/j.mrfmmm.2022.111801","DOIUrl":null,"url":null,"abstract":"<div><h3>Purpose</h3><p>The study objects were to explore the correlation between the biological role of clock genes and clinical indicators in patients with osteosarcoma (OS).</p></div><div><h3>Methods</h3><p>We acquired the clinical information and RNA sequencing data of OS samples from the TARGET database. The protein-protein interaction (PPI) network and expression correlation analysis of clock genes were performed. Then, the functional enrichment analysis of clock genes was analyzed. The survival analysis of clock genes in patients of OS was carried out by univariate cox regression, Kaplan-Meier (KM) curve and multivariate cox regression methods. Moreover, the spearmen correlation analysis was performed to explore the correlation between clock genes and DNA repair genes in patients with OS.</p></div><div><h3>Results</h3><p>The PPI network and expression correlation analysis of clock genes indicated that the clock genes were highly correlated with each other. The survival analysis of clock genes found that clock gene ARNTL is a protective factor for the prognosis of patients with OS. We found that ARNTL was positively related to DNA repair genes and was involved in the biological process of DNA damage repair in patients with OS.</p></div><div><h3>Conclusions</h3><p>ARNTL may affect the prognosis and chemotherapy response of patients with OS by regulating DNA repair pathways.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"825 ","pages":"Article 111801"},"PeriodicalIF":1.5000,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0027510722000288/pdfft?md5=13f06852b07c7c6e96e107eb436d3a72&pid=1-s2.0-S0027510722000288-main.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0027510722000288","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}

引用次数: 1

Abstract

Purpose

The study objects were to explore the correlation between the biological role of clock genes and clinical indicators in patients with osteosarcoma (OS).

Methods

We acquired the clinical information and RNA sequencing data of OS samples from the TARGET database. The protein-protein interaction (PPI) network and expression correlation analysis of clock genes were performed. Then, the functional enrichment analysis of clock genes was analyzed. The survival analysis of clock genes in patients of OS was carried out by univariate cox regression, Kaplan-Meier (KM) curve and multivariate cox regression methods. Moreover, the spearmen correlation analysis was performed to explore the correlation between clock genes and DNA repair genes in patients with OS.

Results

The PPI network and expression correlation analysis of clock genes indicated that the clock genes were highly correlated with each other. The survival analysis of clock genes found that clock gene ARNTL is a protective factor for the prognosis of patients with OS. We found that ARNTL was positively related to DNA repair genes and was involved in the biological process of DNA damage repair in patients with OS.

Conclusions

ARNTL may affect the prognosis and chemotherapy response of patients with OS by regulating DNA repair pathways.

查看原文本刊更多论文

与DNA修复基因相关的生物钟基因ARNTL的表达与骨肉瘤患者的预后

目的探讨骨肉瘤(OS)患者生物钟基因的生物学作用与临床指标的相关性。方法从TARGET数据库中获取OS标本的临床资料和RNA测序数据。对时钟基因进行蛋白-蛋白相互作用(PPI)网络和表达相关性分析。然后，对时钟基因进行功能富集分析。采用单因素cox回归、Kaplan-Meier (KM)曲线和多因素cox回归分析OS患者时钟基因的生存情况。此外，我们还进行spearman相关分析，探讨OS患者时钟基因与DNA修复基因之间的相关性。结果时钟基因的PPI网络和表达相关性分析表明，时钟基因之间存在高度相关性。时钟基因的生存分析发现，时钟基因ARNTL是OS患者预后的保护因素。我们发现ARNTL与DNA修复基因呈正相关，参与了OS患者DNA损伤修复的生物学过程。结论sarntl可能通过调节DNA修复通路影响OS患者的预后和化疗反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.