期刊
CANCER CELL
卷 15, 期 6, 页码 477-488出版社
CELL PRESS
DOI: 10.1016/j.ccr.2009.04.002
关键词
-
资金
- U.S. Veterans Affairs Office of Research and Development
- National Institutes of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases [AR43799, AR49737]
To elucidate mechanisms of cancer progression, we generated inducible human neoplasia. in three-dimensionally intact epithelial tissue. Gene expression profiling of both epithelia and stroma at specific time points during tumor progression revealed sequential enrichment of genes mediating discrete biologic functions in each tissue compartment. A core cancer progression signature was distilled using the increased signaling specificity of downstream oncogene effectors and subjected to network modeling. Network topology predicted that tumor development depends on specific extracellular matrix-interacting network hubs. Blockade of one such hub, the beta 1 integrin subunit, disrupted network gene expression and attenuated tumorigenesis in vivo. Thus, integrating network modeling and temporal gene expression analysis of inducible human neoplasia. provides an approach to prioritize and characterize genes functioning in cancer progression.
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