MNNG-Regulated Differentially Expressed Genes that Contribute to Cancer Development in Stomach Cells
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초록
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.
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.
참고문헌 (18)
- 홍세리, "Cancer Statistics in Korea: Incidence, Mortality, Survival, and Prevalence in 2018", Cancer Research and Treatment, 53(2), pp.301~315 (2021), 대한암학회[DOI]
- Sugimura T, "Tumour production in glandular stomach of rat by N-methyl-N'-nitro-N-nitrosoguanidine", Nature, 216, pp.943~944 (1967)
- Lin L, "Chronic CagA-positive Helicobacter pylori infection with MNNG stimulation synergistically induces mesenchymal and cancer stem cell-like properties in gastric mucosal epithelial cells", J Cell Biochem, 120, pp.17635~17649 (2019)[DOI]
- Kobori O, "Biochemical study of the position specificity of rat gastrointestinal cancer induced by MNNG", Nihon Shokakibyo Gakkai Zasshi, 81, pp.277~ (1984)
- Hamidreza Miri, "A Noninvasive Method for Early Detection of MNNG-Induced Gastric Cancer of Male Wistar rat: Ultrasonic Study", Ultrasound in Medicine & Biology, 37(5), pp.780~787 (2011), Elsevier BV[DOI]
- Deng X, "Protective effect and mechanisms of Weining granule on N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric cancer in rats", J Tradit Chin Med, 39, pp.393~401 (2019)
- Zhang Y, "Synergism of HPV and MNNG repress miR-218 promoting Het-1A cell malignant transformation by targeting GAB2", Toxicology, 447, pp.152635~ (2021)[DOI]
- Szklarczyk D, "STRING v10 : protein-protein interaction networks, integrated over the tree of life", Nucleic Acids Res, 43, pp.D447~D452 (2015)[DOI]
- Sager R, "Expression genetics in cancer : shifting the focus from DNA to RNA", Proc Natl Acad Sci USA, 94, pp.952~955 (1997)[DOI]
- Cai J, "N-methyl-N-nitro-N '-nitrosoguanidine induces the expression of CCR2in human gastric epithelial cells promoting CCL2-mediated migration", Mol Med Rep, 13, pp.1083~1090 (2016)[DOI]
- Bralow SP, "Adenocarcinoma of glandular stomach and duodenum in Wistar rats ingesting N-methyl-N'-nitro-N-nitrosoguanidine, histopathology and associated secretory changes", Cancer Res, 30, pp.1215~1222 (1970)
- Abe M, "Global expression analysis of N-methyl-N'-nitro-N-nitrosoguanidine-induced rat stomach carcinomas using oligonucleotide microarrays", Carcinogenesis, 24, pp.861~867 (2003)[DOI]
- Yuan F, "Analysis of protein-protein functional associations by using gene ontology and KEGG pathway", Biomed Research International, pp.4963289~ (2019)[DOI]
- Szklarczyk D, "STRING v11 : protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets", Nucleic Acids Res, 47, pp.D607~D613 (2019)[DOI]
- Tarkkonen KM, "Differential roles of fibroblast growth factor receptors(FGFR)1, 2 and 3 in the regulation of S115 breast cancer cell growth", PLoS One, 7, pp.e49970~ (2012)[DOI]
- Herbst RS, "Review of epidermal growth factor receptor biology", Int J Radiat Oncol Biol Phys, 59, pp.21~26 (2004)[DOI]
- Milligan G, "Heterotrimeric G-proteins : a short history", Br J Pharmacol, 147, pp.S46~S55 (2006)[DOI]
- Goodfellow PJ, "Assignment of the gene encoding the beta-subunit of the human fibronectin receptor (beta-FNR) to chromosome 10p11.2", Ann Hum Genet, 53, pp.15~22 (1989)[DOI]