High expression of TRIP13 is associated with tumor progression in H. pylori infection induced gastric cancer

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2024-01-01 DOI:10.1016/j.mrfmmm.2024.111854

Longxiang Wu , Qiu Xue , Xiaochun Xia

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引用次数: 0

Abstract

Background/objective

H. pylori is a recognized bacterial carcinogen in the world to cause gastric cancer (GC). However, the molecular mechanism of H. pylori infection-induced GC is not completely clear. Thus, there is an urgent need to reveal the precise mechanisms regulating cancer development due to H. pylori infection.

Methods

GEO microarray databases and TCGA databases were extracted for the analysis of different expression genes (DEGs). Then, Kaplan-Meier Plotter was used for prognostic analysis. Functional enrichment analysis of TRIP13 was performed by metascape database and TIMER database. Specific role of TRIP13 in GC with H. pylori infection was confirmed by CCK8, cell cycle analysis and WB.

Results

A total 10 DEGs were substantially elevated in GC and H. pylori+ tissues and might be associated with H. pylori infection in GC and only the highly expressed TRIP13 was statistically associated with poor prognosis in GC patients. Meanwhile, TRIP13 were upregulated in both CagA-transfected epithelial cells and GC cells. And TRIP13 deficiency inhibited cell proliferation and arrested the cell cycle at the G1 phase.

Conclusion

Our study suggested that high expression of TRIP13 can promote the proliferation, cell cycle in GC cells, which could be used as a biomarker for H. pylori infection GC.

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在幽门螺杆菌感染诱发的胃癌中，TRIP13的高表达与肿瘤进展有关

背景/目的幽门螺杆菌是世界公认的导致胃癌（GC）的细菌致癌物。然而，幽门螺杆菌感染诱发胃癌的分子机制尚不完全清楚。方法提取 GEO 微阵列数据库和 TCGA 数据库，分析不同表达基因（DEGs）。然后使用 Kaplan-Meier Plotter 进行预后分析。metascape数据库和TIMER数据库对TRIP13进行了功能富集分析。结果共有10个DEGs在GC和幽门螺杆菌+组织中显著升高，可能与GC中的幽门螺杆菌感染有关，只有高表达的TRIP13与GC患者的不良预后有统计学相关性。同时，TRIP13在CagA转染的上皮细胞和GC细胞中均上调。结论：我们的研究表明，TRIP13的高表达可促进GC细胞的增殖和细胞周期，可作为幽门螺杆菌感染GC的生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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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.