{"title":"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","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":"{\"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}","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}
Expression of the Circadian Clock Gene ARNTL associated with DNA repair gene and prognosis of patient with osteosarcoma
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.
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.
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