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长期饮用南京自来水导致小鼠肝癌形成过程中的信号转导障碍。

Signal transduction disturbance related to hepatocarcinogenesis in mouse by prolonged exposure to Nanjing drinking water.

机构信息

State Key Laboratory of Pollution Control & Resource Reuse, School of the Environment, Nanjing University, 163 Xianlin Road, Nanjing, 210046, People's Republic of China.

出版信息

Environ Sci Pollut Res Int. 2013 Sep;20(9):6468-81. doi: 10.1007/s11356-013-1695-9. Epub 2013 Apr 17.

Abstract

Toxicogenomic approaches were used to investigate the potential hepatocarcinogenic effects on mice by oral exposure to Nanjing drinking water (NJDW). Changes in the hepatic transcriptome of 3 weeks male mice (Mus musculus) were monitored and dissected after oral exposure to NJDW for 90 days. No preneoplastic and neoplastic lesions were observed in the hepatic tissue by the end of NJDW exposure. However, total of 746 genes were changed transcriptionally. Thirty-one percent of differentially expressed genes (DEGs) were associated with the functional categories of cell cycle regulation, adhesion, growth, apoptosis, and signal transduction, which are closely implicated in tumorigenesis and progression. Interrogation of Kyoto Encyclopedia of Genes and Genomes revealed that 43 DEGs were mapped to several crucial signaling pathways implicated in the pathogenesis of hepatocellular carcinoma (HCC). In signal transduction network constructed via Genes2Networks software, Egfr, Akt1, Atf2, Ctnnb1, Hras, Mapk1, Smad2, and Ccnd1 were hubs. Direct gene-disease relationships obtained from Comparative Toxicogenomics Database and scientific literatures revealed that the hubs have direct mechanism or biomarker relationships with hepatocellular preneoplastic lesions or hepatocarcinogenesis. Therefore, prolonged intake of NJDW without employing any indoor water treatment strategy might predispose mouse to HCC. Furthermore, Egfr, Akt1, Ctnnb1, Hras, Mapk1, Smad2, and Ccnd1 were identified as promising biomarkers of the potential combined hepatocarcinogenicity.

摘要

毒理基因组学方法被用于研究南京饮用水(NJDW)经口服暴露对小鼠的潜在肝致癌作用。监测了雄性小鼠(Mus musculus)经口服暴露 90 天后的肝转录组变化,并对其进行了分析。在 NJDW 暴露结束时,肝组织中未观察到任何前瘤性和肿瘤性病变。然而,共有 746 个基因的转录发生了变化。31%的差异表达基因(DEGs)与细胞周期调控、黏附、生长、凋亡和信号转导等功能类别相关,这些功能类别与肿瘤发生和进展密切相关。京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes)的查询结果显示,43 个 DEGs 映射到几个与肝细胞癌(HCC)发病机制相关的关键信号通路。通过 Genes2Networks 软件构建的信号转导网络中,Egfr、Akt1、Atf2、Ctnnb1、Hras、Mapk1、Smad2 和 Ccnd1 是枢纽基因。从比较毒理学基因组数据库和科学文献中获得的直接基因-疾病关系表明,这些枢纽基因与肝细胞前瘤性病变或肝癌发生具有直接的机制或生物标志物关系。因此,长期摄入未经任何室内水处理策略处理的 NJDW 可能使小鼠易患 HCC。此外,Egfr、Akt1、Ctnnb1、Hras、Mapk1、Smad2 和 Ccnd1 被确定为潜在联合致癌作用的有前途的生物标志物。

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