Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Mol Cell. 2009 Dec 11;36(5):900-11. doi: 10.1016/j.molcel.2009.11.016.
The discovery of pathways and regulatory networks whose perturbation contributes to neoplastic transformation remains a fundamental challenge for cancer biology. We show that such pathway perturbations, and the cis-regulatory elements through which they operate, can be efficiently extracted from global gene expression profiles. Our approach utilizes information-theoretic analysis of expression levels, pathways, and genomic sequences. Analysis across a diverse set of human cancers reveals the majority of previously known cancer pathways. Through de novo motif discovery we associate these pathways with transcription-factor binding sites and miRNA targets, including those of E2F, NF-Y, p53, and let-7. Follow-up experiments confirmed that these predictions correspond to functional in vivo regulatory interactions. Strikingly, the majority of the perturbations, associated with putative cis-regulatory elements, fall outside of known cancer pathways. Our study provides a systems-level dissection of regulatory perturbations in cancer-an essential component of a rational strategy for therapeutic intervention and drug-target discovery.
通路和调控网络的发现,其干扰有助于肿瘤的转化,这仍然是癌症生物学的一个基本挑战。我们表明,这些通路的干扰,以及它们作用的顺式调控元件,可以从全局基因表达谱中有效地提取出来。我们的方法利用了表达水平、通路和基因组序列的信息论分析。在一组多样化的人类癌症中进行的分析揭示了大多数先前已知的癌症通路。通过从头发现基序,我们将这些通路与转录因子结合位点和 miRNA 靶标联系起来,包括 E2F、NF-Y、p53 和 let-7。后续实验证实,这些预测对应于体内功能性调控相互作用。引人注目的是,与假定的顺式调控元件相关的大多数干扰都不在已知的癌症通路范围内。我们的研究提供了癌症调控干扰的系统水平剖析——这是治疗干预和药物靶点发现的合理策略的一个重要组成部分。