Modeling inducible human tissue neoplasia identifies an extracellular matrix interaction network involved in cancer progression
Open accessAbstract
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 beta1 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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ITGB1 and CD151 are pro-tumorigenic by enhancing cell migration and stromal invasion.
“ITGB1 and CD151 are known to be pro-tumorigenic by enhancing cell migration and stromal invasion (Reuter et al., 2009, White et al., 2004, Yang et al., 2008, Zijlstra et al., 2008).”
From Multimodal Analysis of Composition and Spatial Architecture in Human Squamous Cell Carcinoma (2020) · cites this paper as Reuter et al., 2009
The Results section (page unavailable) supports a pro-tumorigenic role for β1 integrin (ITGB1) in Ras-driven epidermal tumors, including invasion: β1 inhibition reduced tumor growth and produced a clearer tumor–stroma border. The retrieved passages do not establish that ITGB1 enhances cell migration, and a search for CD151 found no passage supporting a role for it. (LLM, conf=0.86)
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References 53 · Cited by 88
- Authors
- Reuter, J. A., Ortiz-Urda, S., Kretz, M., Garcia, J., Scholl, F. A., Pasmooij, A. M. G., Cassarino, D., Chang, H. Y., & Khavari, P. A.
- Affiliations
- VA Palo Alto Health Care System (US)
- University of California, Los Angeles (US)
- Stanford Medicine (US)
- Corresponding author
- Khavari, Paul A.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 15
- Issue
- 6
- Pages
- 477-488
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3050547
- OpenAlex
- W2104278772
- Cited by
- 88
- References
- 53
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 1 · 2023: 5 · 2022: 6 · 2021: 8 · 2020: 5 · 2019: 6 · 2018: 2 · 2017: 5 · 2016: 2 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 9
- FWCI
- 4.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK62027, R01DK062027)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR049737, R01AR043799)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- tumor progression, extracellular matrix, beta1 integrin, network modeling, gene expression profiling, tumor stroma, epithelium, network hubs, oncogene signaling
- MeSH terms
- Animals, Carcinoma, Squamous Cell, Cell Line, Cell Transformation, Neoplastic, Epithelial Cells, Extracellular Matrix, Female, Humans, Models, Biological, Neoplasm Invasiveness, Neoplasm Transplantation, Skin Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Mice, SCID, Stromal Cells, Integrin beta1, Oligonucleotide Array Sequence Analysis, Protein Interaction Mapping, Mice
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