MNNG-Regulated Differentially Expressed Genes that Contribute to Cancer Development in Stomach Cells

Tae-Jin Kim, Myeong-Kwan Kim, Dongju Jung
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引用次数: 1

Abstract

Cancer is a global health problem. There are diverse types of cancers, but there are several common pathways which lead to the development of cancer. Changes in gene expression might be the most common similarity found in almost all cancers. An understanding of the underlying changes in gene expression during cancer progression could lay a valuable foundation for the development of cancer therapeutics and even cancer vaccines. In this study, a well-known carcinogen, N-methyl-N’-nitro-N-nitrosoguanidine (MNNG), was employed to induce changes in gene expression in normal stomach cells. MNNG is known to cause cancer by inducing damage to DNA in MNNG-treated mammalian cells and animals fed with this carcinogen. An analysis was performed by comparing the differentially expressed genes (DEGs) caused by MNNG treatment with DEGs in stomach cancer cell lines. To this end, methods of analysis for functional categorization and protein-protein interaction networks, such as gene ontology (GO), the database for annotation, visualization, and integrated discovery (DAVID), Kyoto encyclopedia of genes and genomics (KEGG) and search tool for the retrieval of interacting genes/proteins (STRING), were used. As a result of these analyses, MNNG-regulated specific genes and interaction networks of their protein products that contributed to stomach cancer were identified. Copyright Ⓒ
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胃癌细胞中mnng调控的差异表达基因
癌症是一个全球健康问题。癌症有多种类型,但有几种常见的途径导致癌症的发展。基因表达的变化可能是几乎所有癌症中最常见的相似之处。了解癌症进展过程中基因表达的潜在变化可以为癌症治疗甚至癌症疫苗的发展奠定宝贵的基础。在这项研究中,我们使用了一种众所周知的致癌物质n -甲基-n ' -硝基-n -亚硝基胍(MNNG)来诱导正常胃细胞的基因表达变化。已知MNNG通过诱导MNNG处理的哺乳动物细胞和喂食这种致癌物的动物的DNA损伤而致癌。通过比较MNNG处理引起的胃癌细胞系差异表达基因(DEGs)和DEGs进行了分析。为此,使用了功能分类和蛋白质-蛋白质相互作用网络的分析方法,如基因本体(GO)、注释、可视化和集成发现数据库(DAVID)、京都基因与基因组百科全书(KEGG)和相互作用基因/蛋白质检索工具(STRING)。通过这些分析,确定了mnng调节的特定基因及其蛋白质产物的相互作用网络,这些基因和相互作用网络有助于胃癌。版权Ⓒ
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发文量
29
审稿时长
8 weeks
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