Pendse Salil N, Maertens Alexandra, Rosenberg Michael, Roy Dipanwita, Fasani Rick A, Vantangoli Marguerite M, Madnick Samantha J, Boekelheide Kim, Fornace Albert J, Odwin Shelly-Ann, Yager James D, Hartung Thomas, Andersen Melvin E, McMullen Patrick D
The Hamner Institutes for Health Sciences, Research Triangle Park, NC, USA.
ScitoVation, LLC, 6 Davis Drive, PO Box 110566, Research Triangle Park, NC, 27709, USA.
Arch Toxicol. 2017 Apr;91(4):1749-1762. doi: 10.1007/s00204-016-1824-6. Epub 2016 Sep 3.
The twenty-first century vision for toxicology involves a transition away from high-dose animal studies to in vitro and computational models (NRC in Toxicity testing in the 21st century: a vision and a strategy, The National Academies Press, Washington, DC, 2007). This transition requires mapping pathways of toxicity by understanding how in vitro systems respond to chemical perturbation. Uncovering transcription factors/signaling networks responsible for gene expression patterns is essential for defining pathways of toxicity, and ultimately, for determining the chemical modes of action through which a toxicant acts. Traditionally, transcription factor identification is achieved via chromatin immunoprecipitation studies and summarized by calculating which transcription factors are statistically associated with up- and downregulated genes. These lists are commonly determined via statistical or fold-change cutoffs, a procedure that is sensitive to statistical power and may not be as useful for determining transcription factor associations. To move away from an arbitrary statistical or fold-change-based cutoff, we developed, in the context of the Mapping the Human Toxome project, an enrichment paradigm called information-dependent enrichment analysis (IDEA) to guide identification of the transcription factor network. We used a test case of activation in MCF-7 cells by 17β estradiol (E2). Using this new approach, we established a time course for transcriptional and functional responses to E2. ERα and ERβ were associated with short-term transcriptional changes in response to E2. Sustained exposure led to recruitment of additional transcription factors and alteration of cell cycle machinery. TFAP2C and SOX2 were the transcription factors most highly correlated with dose. E2F7, E2F1, and Foxm1, which are involved in cell proliferation, were enriched only at 24 h. IDEA should be useful for identifying candidate pathways of toxicity. IDEA outperforms gene set enrichment analysis (GSEA) and provides similar results to weighted gene correlation network analysis, a platform that helps to identify genes not annotated to pathways.
21世纪毒理学的愿景是从高剂量动物研究转向体外和计算模型(美国国家研究委员会,《21世纪毒性测试:愿景与战略》,美国国家科学院出版社,华盛顿特区,2007年)。这种转变需要通过了解体外系统对化学扰动的反应来绘制毒性途径。揭示负责基因表达模式的转录因子/信号网络对于定义毒性途径至关重要,最终对于确定毒物作用的化学作用模式也至关重要。传统上,转录因子的鉴定是通过染色质免疫沉淀研究实现的,并通过计算哪些转录因子与上调和下调基因在统计学上相关来进行总结。这些列表通常通过统计或倍数变化阈值来确定,这一过程对统计功效敏感,可能对确定转录因子关联不太有用。为了摆脱基于任意统计或倍数变化的阈值,我们在“绘制人类毒物组”项目的背景下开发了一种名为信息依赖富集分析(IDEA)的富集范式,以指导转录因子网络的鉴定。我们使用了17β-雌二醇(E2)激活MCF-7细胞的测试案例。使用这种新方法,我们建立了对E2的转录和功能反应的时间进程。ERα和ERβ与对E2的短期转录变化相关。持续暴露导致额外转录因子的募集和细胞周期机制的改变。TFAP2C和SOX2是与剂量相关性最高的转录因子。参与细胞增殖的E2F7、E2F1和Foxm1仅在24小时时富集。IDEA应该有助于识别毒性候选途径。IDEA优于基因集富集分析(GSEA),并提供与加权基因共表达网络分析类似的结果,加权基因共表达网络分析是一个有助于识别未注释到途径的基因的平台。