Suppr超能文献

揭示人类癌症中全球调控扰动。

Revealing global regulatory perturbations across human cancers.

机构信息

Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.

出版信息

Mol Cell. 2009 Dec 11;36(5):900-11. doi: 10.1016/j.molcel.2009.11.016.

Abstract

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.

摘要

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。

相似文献

1
Revealing global regulatory perturbations across human cancers.
Mol Cell. 2009 Dec 11;36(5):900-11. doi: 10.1016/j.molcel.2009.11.016.
2
A FIRE-y PAGE in the computational analysis of cancer profiles.
Mol Cell. 2009 Dec 11;36(5):732-3. doi: 10.1016/j.molcel.2009.11.019.
3
Investigation of key miRNAs and target genes in bladder cancer using miRNA profiling and bioinformatic tools.
Mol Biol Rep. 2014 Dec;41(12):8127-35. doi: 10.1007/s11033-014-3713-5. Epub 2014 Sep 5.
4
Integrative microRNA and mRNA deep-sequencing expression profiling in endemic Burkitt lymphoma.
BMC Cancer. 2017 Nov 13;17(1):761. doi: 10.1186/s12885-017-3711-9.
6
CompMoby: comparative MobyDick for detection of cis-regulatory motifs.
BMC Bioinformatics. 2008 Oct 27;9:455. doi: 10.1186/1471-2105-9-455.
7
LncMAP: Pan-cancer atlas of long noncoding RNA-mediated transcriptional network perturbations.
Nucleic Acids Res. 2018 Feb 16;46(3):1113-1123. doi: 10.1093/nar/gkx1311.
8
Molecular subtypes of urothelial carcinoma are defined by specific gene regulatory systems.
BMC Med Genomics. 2015 May 26;8:25. doi: 10.1186/s12920-015-0101-5.
9
Screening candidate genes associated with bladder cancer using DNA microarray.
Mol Med Rep. 2014 Dec;10(6):3087-91. doi: 10.3892/mmr.2014.2667. Epub 2014 Oct 15.
10
Identification of candidate B-lymphoma genes by cross-species gene expression profiling.
PLoS One. 2013 Oct 9;8(10):e76889. doi: 10.1371/journal.pone.0076889. eCollection 2013.

引用本文的文献

2
DNA methylation affects gene expression but not global chromatin structure in .
J Bacteriol. 2025 Jul 14:e0054024. doi: 10.1128/jb.00540-24.
4
HP-Bodies - Ancestral Condensates that Regulate RNA Turnover and Protein Translation in Bacteria.
bioRxiv. 2025 Feb 6:2025.02.06.636932. doi: 10.1101/2025.02.06.636932.
5
DNA methylation affects gene expression but not global chromatin structure in .
bioRxiv. 2025 Jan 19:2025.01.06.631547. doi: 10.1101/2025.01.06.631547.
6
A generative framework for enhanced cell-type specificity in rationally designed mRNAs.
bioRxiv. 2024 Dec 31:2024.12.31.630783. doi: 10.1101/2024.12.31.630783.
7
Identification and genetic dissection of convergent persister cell states.
Nature. 2024 Dec;636(8042):438-446. doi: 10.1038/s41586-024-08124-2. Epub 2024 Nov 6.
8
A multiomics approach reveals RNA dynamics promote cellular sensitivity to DNA hypomethylation.
Sci Rep. 2024 Oct 29;14(1):25940. doi: 10.1038/s41598-024-77314-9.
10
Integrative identification of non-coding regulatory regions driving metastatic prostate cancer.
Cell Rep. 2024 Sep 24;43(9):114764. doi: 10.1016/j.celrep.2024.114764. Epub 2024 Sep 13.

本文引用的文献

1
Microarray profiling of phage-display selections for rapid mapping of transcription factor-DNA interactions.
PLoS Genet. 2009 Apr;5(4):e1000449. doi: 10.1371/journal.pgen.1000449. Epub 2009 Apr 10.
2
Vascular endothelial growth factor expression in ovarian cancer: a model for targeted use of novel therapies?
Clin Cancer Res. 2008 May 15;14(10):3030-5. doi: 10.1158/1078-0432.CCR-07-1888.
3
Genetic variations of microRNAs in human cancer and their effects on the expression of miRNAs.
Carcinogenesis. 2008 Sep;29(9):1710-6. doi: 10.1093/carcin/bgn073. Epub 2008 Mar 19.
4
Systematic functional characterization of cis-regulatory motifs in human core promoters.
Genome Res. 2008 Mar;18(3):477-88. doi: 10.1101/gr.6828808. Epub 2008 Feb 6.
5
Endogenous human microRNAs that suppress breast cancer metastasis.
Nature. 2008 Jan 10;451(7175):147-52. doi: 10.1038/nature06487.
6
miRBase: tools for microRNA genomics.
Nucleic Acids Res. 2008 Jan;36(Database issue):D154-8. doi: 10.1093/nar/gkm952. Epub 2007 Nov 8.
7
A universal framework for regulatory element discovery across all genomes and data types.
Mol Cell. 2007 Oct 26;28(2):337-50. doi: 10.1016/j.molcel.2007.09.027.
8
The let-7 microRNA represses cell proliferation pathways in human cells.
Cancer Res. 2007 Aug 15;67(16):7713-22. doi: 10.1158/0008-5472.CAN-07-1083.
9
Targeting c-Jun and JunB proteins as potential anticancer cell therapy.
Oncogene. 2008 Jan 24;27(5):641-52. doi: 10.1038/sj.onc.1210690. Epub 2007 Jul 30.
10
The p53 family in differentiation and tumorigenesis.
Nat Rev Cancer. 2007 Mar;7(3):165-8. doi: 10.1038/nrc2072. Epub 2007 Feb 1.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验