Zeller Karen I, Zhao XiaoDong, Lee Charlie W H, Chiu Kuo Ping, Yao Fei, Yustein Jason T, Ooi Hong Sain, Orlov Yuriy L, Shahab Atif, Yong How Choong, Fu Yutao, Weng Zhiping, Kuznetsov Vladimir A, Sung Wing-Kin, Ruan Yijun, Dang Chi V, Wei Chia-Lin
Department of Medicine and The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Proc Natl Acad Sci U S A. 2006 Nov 21;103(47):17834-9. doi: 10.1073/pnas.0604129103. Epub 2006 Nov 8.
The protooncogene MYC encodes the c-Myc transcription factor that regulates cell growth, cell proliferation, cell cycle, and apoptosis. Although deregulation of MYC contributes to tumorigenesis, it is still unclear what direct Myc-induced transcriptomes promote cell transformation. Here we provide a snapshot of genome-wide, unbiased characterization of direct Myc binding targets in a model of human B lymphoid tumor using ChIP coupled with pair-end ditag sequencing analysis (ChIP-PET). Myc potentially occupies > 4,000 genomic loci with the majority near proximal promoter regions associated frequently with CpG islands. Using gene expression profiles with ChIP-PET, we identified 668 direct Myc-regulated gene targets, including 48 transcription factors, indicating that Myc is a central transcriptional hub in growth and proliferation control. This first global genomic view of Myc binding sites yields insights of transcriptional circuitries and cis regulatory modules involving Myc and provides a substantial framework for our understanding of mechanisms of Myc-induced tumorigenesis.
原癌基因MYC编码c-Myc转录因子,该因子可调节细胞生长、细胞增殖、细胞周期和细胞凋亡。尽管MYC失调会导致肿瘤发生,但目前仍不清楚Myc直接诱导的转录组是如何促进细胞转化的。在此,我们通过染色质免疫沉淀结合双末端标签测序分析(ChIP-PET),对人B淋巴细胞瘤模型中Myc的直接结合靶点进行了全基因组、无偏倚的特征描述。Myc可能占据了超过4000个基因组位点,其中大多数位于与CpG岛频繁相关的近端启动子区域附近。通过结合ChIP-PET的基因表达谱,我们鉴定出668个Myc直接调控的基因靶点,其中包括48个转录因子,这表明Myc是生长和增殖控制中的一个核心转录枢纽。对Myc结合位点的这一首次全局基因组观察,揭示了涉及Myc的转录调控网络和顺式调控模块,并为我们理解Myc诱导肿瘤发生的机制提供了一个坚实的框架。