Gene expression profiling in human lung fibroblast following cadmium exposure
Gene expression profiling in human lung fibroblast following cadmium exposure
复制标题
DOI：
10.1016/j.fct.2007.11.007
复制
发表时间：
2008-03-01
影响因子：
4.3
通讯作者：
Lee, Byung-Hoon
中科院分区：
文献类型：
--
作者：
Li, Guang-Yong;Kim, Mingoo;Lee, Byung-Hoon
镉是一种天然存在的金属元素，食物和吸烟是非职业接触人群的主要接触源。长期接触镉会导致包括肺在内的许多组织发生肿瘤。在本研究中，我们研究了基因的表达被镉暴露在人肺成纤维细胞W138-VA 13细胞的修改。我们采用了cDNA微阵列杂交方法，以确定基因表达谱的变化。35个基因被鉴定为镉响应基因。它们的表达水平与对照显著不同（微阵列的显著性分析; SAM，q < 5%）。受镉暴露影响最大的基因产物组是那些参与细胞周期，免疫和防御，核苷代谢和信号转导。镉暴露后E2 f1、Tubb和Actg 2的表达受到抑制，可能与细胞周期阻滞有关。Enol的下调表明可能导致原癌基因表达，并可能导致镉诱导的致癌性。这些结果可能有助于更好地理解镉毒性的毒性机制。此外，镉的基因表达谱可以为镉暴露提供潜在的生物标志物。(c)2007爱思唯尔有限公司保留所有权利。
Cadmium is a naturally occurring metallic element with food and smoking being the main sources of exposure in the non-occupationally exposed population. Chronic exposure to cadmium leads to tumors in a number of tissues including lung. In the present study we investigated genes whose expression is modified by Cd exposure in human lung fibroblast W138-VA13 cells. We employed a cDNA microarray hybridization method to identify changes in the gene expression profile. Thirty five genes were identified as cadmium-responsive. Their level of expression differed significantly from controls (significance analysis of microarray; SAM, q < 5%). The largest groups of gene products affected by cadmium exposure were those involved in cell cycle, immunity and defense, nucleoside metabolism and signal transduction. Repressed expression of E2f1, Tubb and Actg2 following cadmium exposure may contribute to the cell cycle arrest. Down-regulation of Enol indicates a potential for causing protooncogene expression and possibly for cadmium-induced carcinogenicity. These results may contribute to better understand the toxic mechanism of cadmium toxicity. Moreover, the gene expression profile of cadmium could provide potential biomarkers for cadmium exposure. (c) 2007 Elsevier Ltd. All rights reserved.